Acute and Chronic Complication of Diabetes.pptx

ACUTE AND CHRONIC
COMPLICATIONS OF DIABETES
Dr Raja Mustafa
ROYAL CARE INTERNATIONAL HOSPITAL
(KHARTOUM---- SUDAN)
RWANDA MILITARY HOSPITAL

COMPLICATIONS
A) ACUTE ( Emergency ):
1) Hypoglycaemia
2) Diabetic Hyperglycaemic Emergencies
a) Diabetic ketoacidosis ( DKA )
b) Hyperosmolar Hyperglycaemic state ( HHS )

B) Chronic complications of DM
1) Microvascular complications
2) Macrovascular complications

Definition
• Diabetes mellitus (DM) is a metabolic disorder characterized
by chronic hyperglycaemia due to defects in insulin secretion
and/or insulin action .
• These conditions are associated with disordered carbohydrate ,
fat , and protein metabolism and can lead to long-term
complications involving the nervous, cardiovascular, renal systems.

• According to International Diabetes Federation ( IDF )
statistic- 2022 , 463 million people affected globally and the numbers
will rise to 550 million by year 2030.

WHO glucose thresholds Criteria for diagnosis of Diabetes Mellitus
1) Fasting Blood Glucose
Fasting is defined as no caloric intake for at least 8h to 12h.
≥ 7.0mmol/l or > 126mg/dl
2) 2hr after 75g OGTT ≥11.1mmol/l or > 200mg/dl
3) Random Blood Glucose ≥11.1mmol/l or > 200mg/dl
4) HbA1C1 ≥ 6.5 % (48mmol/mol)
NB : repeat test twice for asymptomatic patients
Single high test is sufficient for diagnosis in symptomatic patients

Pre - Diabetes
 Impaired glucose tolerance ( IGT)
2hr glucose during an OGTT ( ≥7.8 and <11.1 mmol/l)
 Impaired fasting glucose ( IFG)
Fasting ( ≥6.1 and <7.0 mmol/l )
 HbAlc ≥ 5.7% up to 6.4 %
 Patients with pre-diabetes (HbA1c ≥ 5.7% , IGT or IFG) they have
dominant factor associated with progression to DM so that
should be tested yearly.

1. Development of autonomic or neuroglycopenic symptoms
2. Plasma glucose <70 mg/dL
3. Response to carbohydrate load
Definition of hypoglycemia

Classification of hypoglycemia

• Severe Hypoglycaemia
( Blood glucose level below 27 mg/dL or 1.5 mmol/L )
 It’s an episode of hypoglycaemia that require :
- Assistance from another person
- Hospitalization
- Parental glucose administration
- Treatment with glucagon + Dextrose

Factors that increase the risk of hypoglycemia
• Use of insulin or insulin secretagogues e.g SUs
• Impaired renal or hepatic function
• Long duration of diabetes
• Frailty and old age
• Cognitive impairment
• Impaired counter-regulatory response e.g hypoglycemia unawareness
• Polypharmacy
• Tight glycaemic control

Adrenergic Neuroglycopenic
Trembling Dizziness --- Drowsiness
Palpitations Weakness
Sweating Difficulty concentrating
Anxiety Visual change
Hunger Difficulty in speech
Nausea Seizures
Drowsiness
Symptoms of hypoglycemia

Investigations :
- Random blood glucose
- Fasting blood glucose
- Oral glucose tolerance test
- Renal function test and electrolytes
- Liver function test
- Complete blood count
- Serum insulin level and C- peptide
- Serum cortisol
- Imaging CT or MRI

20
Treatment of severe hypoglycemia
in an unconscious patient
Give glucagon (SC or IM)

Treatment of severe hypoglycemia in an
unconscious patient
• Treat with 10-25 g of glucose (20-50 mL of Dextrose 50%) intravenously
over 1-3 minutes
• Re-test in 15 minutes to ensure the gluocse >70 mg/dL and re-treat with a
further dose of dextrose 50%
• Once conscious, eat meal or a snack

 Diabetic ketoacidosis is a medical emergency
 DKA is a state of uncontrolled catabolism triggered by a
relative or absolute deficiency in circulating insulin .
Biochemical triad
 Hyperglycaemia
 Ketoacids
 Metabolic acidosis
Diabetic ketoacidosis

 Insulin effect
 Suppression of gluconeogenesis and promoting glycogen synthesis and
storage.
 It promotes the peripheral uptake of glucose , particulary in skeletal
muscles, and encourages storages (as muscle glycogen) and protein synthesis.
 It also promotes lipogenesis and suppresses lipolysis.
 In the absence of insulin , these processes are reversed
PATHOPHYSIOLOGY

 Insulin deficiency is accompanied by a reciprocal elevation in counter regulatory
hormones
(glucagon, epinephrine, growth hormone, and cortisol)
which causes increased glucose production by the liver (gluconeogenesis)
and catabolism of fat (lipolysis).
 Lipolysis provides the substrate (free fatty acids) for the uncontrolled
production of ketones by the liver.
 beta-hydroxybutyrate
 acetoacetate
 acetone
 The production of ketones then leads to metabolic acidosis.

Pathophysiology
Insulin
Counterregulatory hormones
• Glucagon
• Catecholamines
• Cortisol
• Growth hormone
Normal

Pathophysiology
Insulin deficiency
DKA
Counterregulatory hormones
• Glucagon
• Catecholamines
• Cortisol
• Growth hormone

Insulin Deficiency
Glucose uptake
Proteolysis
Lipolysis
Amino Acids
Glycerol Free Fatty Acids
Gluconeogenesis
Glycogenolysis
Hyperglycemia Ketogenesis
Acidosis
Osmotic diuresis
Dehydration
Excess counterregulatory hormones

 Diagnosis
DKA
Hyperglycaemia Acidosis
Ketosis

Blood Glucose < 11mmol/L
< 200 mg /dL
Ketonaemia
ketonuria
more < 3mmol/L ketonaemia
or significant ketonuria ( <2+)
Blood Gases
( Acidosis )
Arterial pH > 7.3
Hco3 > 15 mmol/L
DKA Diagnostic Criteria

 DKA – cause or trigger
Incidence
New-onset diabetes 5-40%
Acute illness 10-20%
Insulin omission/non-adherence 33%
Infection 20-38%
Heart attack, stroke, pancreatitis <10%
Acute stress ( trauma –surgery)
Slides current until 2023
Booth 2020, 2020

35
 History
 Thirst and polyuria
 Nausea / vomiting
 Abdominal pain
 Physical examination
 Tachycardia/ hypotension
 Tachypnoea
 Kussmaul’s respiration (air hunger)
 Dehydration
 Ketotic breath
 Confusion / coma

Immediate for diagnosis
• Capillary blood glucose,
• urine for ketones
• Venous ABG ( PH.. Bicarbonate )
Urgent for assessment and treatment
• Blood glucose … HbAIC
• Complete blood count
• Electrolytes ( Na, K , urea, creatinine
• Mid stream urine
Consider
• Cardiac monitor ( ECG) …
• Blood culture, urine culture
• Chest X-ray
• Urine and blood culture
• BFFM
DKA – Investigations

Ketones
 Blood ketone testing detects beta-hydroxybutyrate
 Blood ketone testing (if available) may enable early identification of DKA and is a
direct marker of disease severity
 Serum B – Hydroxybutyrate is the predominant ketone in untreated DKA
 The usual practice is to test urine for ketones
(acetone and acetoacetate).

Monitoring
Hourly:
 Pulse
 BP
 RR
 Fluid input / output
 Capillary glucose
Four Hourly:
 Potassium
 Bicarbonate
 Urine dipstick for ketones

1) IV fluids
2) IV insulin
3) Potassium replacement
4) Treatment of precipitating cause
5) Anticoagulation
6) Transition to subcutaneous insulin
Management of DKA

 The presence of any of the following should prompt consideration of admission to a level 2/high dependency unit
(HDU) environment:
 Bicarbonate < 5 mmol/L
 pH (venous or arterial) < 7.1
 Glasgow coma scale < 10
 Systolic BP < 90 mmHg
 High anion Gap > 16
( Na+k) – (Cl + Hco3)
 O2 Saturation < 92%
 Blood ketones > 6 mmol/L

 IV fluids

Aims:
 Replace fluid deficit
 Clearance of ketone
 Improve renal function
 0.9% normal saline is the fluid of choice

 IV fluids
Element Rate ml/hour
1st
litre over 1 hour 1000
2nd
litre over 2 hours 500
3rd
4th
5th
Suggested guide for rate of IV saline infusion for
most patients with DKA

 IV fluids
1st
2nd
3rd
4th
5th
Suggested guide for rate of IV saline infusion for
most patients with DKA
5 litres over first
13 hours

 IV fluids
• If systolic BP <90 mmHg, give 500 ml saline over 10-15 minutes
Repeat , if systolic BP still <90 mmHg ( assess for circulatory support)
• When glucose reaches 250 mg/dL, change to 10% dextrose in a rate 125ml/hr
 Slower rates of infusion in:
 >70 years
 Cardiac failure
 Renal failure

 Potassium replacement
If plasma potassium result not available on admission:
• The first 2 bags of 500 ml saline should be without added potassium
• When potassium result known, follow the table below:

 Potassium replacement
If plasma potassium result available quickly on
admission, follow table below:
Serum potassium Potassium chloride/litre fluid
> 5.5 mmol/L Give saline with no added KCl
3.3 - 5.5 mmol/L Add KCl 20 mmol to each 500 ml bag of saline
<3.3 mmol/L Add KCl 20 mmol to each 500 ml bag of saline
and:
- consider increasing rate of infusion if fluid
balance allows
- withhold insulin until potassium 3.3

Insulin Therapy
 Aim
 To correct hyperglycaemia
 To correct acidosis … ketosis
 FRIII
Fixed Rate Intravenous Insulin Infusion
FRIII 0.1U /Kg/hr

Insulin Therapy
If syringe infusion pump available:
 Add 50 units of soluble human insulin to 50 ml normal saline, this gives a
concentration of
1 unit/ml ( 1 unit = 1 ml )
FRIII 0.1U/kg /hr
 Infuse at a fixed rate of 0.1 unit/kg/hour, based on estimating patient’s weight
e.g 80 kg person ( 80 * 0.1) = 8 unit /hr = 8ml /hr
 This should be infused into a separate IV line and the solution should be
changed every 6 hours
 The rate of intravenous insulin infusion may be reduced to 0.05 U/Kg/ hr once blood
glucose drops.

Insulin therapy
If syringe infusion pump is not available:
• Give a subcutaneous injection of soluble human insulin at a dose of
0.1 unit/kg every hour (or 0.2 units/kg every 2 hours)
With both IV or SC regimes:
• Long-acting basal insulin analogs (glargine or detemir) should be
continued

Insulin therapy
 Aim to reduce plasma glucose gradually by 50 -- 70 mg/dL/hour
 If the drop of plasma glucose is less than 50 mg/dL/hour:
increase insulin (IV or SC) dose by 1 unit/hour every hour until target achieved
 If K<3.3 withhold insulin until K ≥ 3.3

 Bicarbonate
 Rarely necessary and usually if pH <6.9
 Hco3 should not be given because it may worsen intracellular acidosis
and precipitate cerebral oedema particulary in children .
 Should be given very cautiously, only in ICU

1] Reduction in blood ketone by 0.5 mmol/L /hr
2] Reduction in Capillary blood glucose by 3.0mmol/L /hr ( 54mg/dl )
3] Increase in venous Hco3 by 3mmol/L /hr
4] Potassium maintained at 4.5 -- 5.5 mmol/L
If these rates are not achieved, then the FRIII needs adjusting.
Metabolic Treatment Targets in DKA

 Blood Glucose < 200mg/dL
 PH > 7.3
 Bicarbonate (Hco3) > 18mmol/L
 Normal anion gap
 Disappearance of ketonuria is not a condition for resolution of DKA:
 Acetone may remain positive in urine up to 36 hours after resolution of DKA and
clearance of the main ketones, beta-hydroxybutyrate and acetoacetate
American Diabetes Association (ADA)
Resolution Criteria of DKA

 Message
• Continue subcutaneous basal insulin as usual on the same time
• Short – acting insulin s/c should be given 30—60 mins before discontinuing
intravenous insulin .
(To avoid recurrence of DKA , subcutaneous insulin allow overlap between
stopping IV insulin infusion and starting s/c insulin) .
• If patient is out of Diabetic ketoacidosis and can’t take oral , due to other co -
morbidities stop fixed rate variable intravenous insulin and start basal insulin plus
(VRIII) variable rate intravenous insulin infusion .

• Restart usual insulin regime
• For newly diagnosed diabetes ( insulin naïve patient), start basal bolus insulin
at a total dose of 0.5-0.8 units/kg/day
e.g 120 kg person weight
120 * 0.5 = 60 unit
( 30 U basal + 30 U regular)
30 unit basal insulin
Regular Human insulin pre meal 10 U –10U– 10 U
 Management of the recovery period from DKA

 Anticoagulation
 Hyperglycaemia and dehydration leads to hyperviscocity
Increase risk of arterial and venous thromboembolism
 LMWH for full duration of admission unless contraindicated

 Complications of DKA
1] Hypokalemia and hyperkalemia
• Can be life-threatening,
• Avoid by regular monitoring and careful potassium replacement
2] Hypoglycemia
• Avoid by giving dextrose 10% when glucose reaches 250 mg/dL
3] Cerebral odema
• Usually in children and adolescents
• Avoid by cautious fluid replacement in young patients
4] Acute kidney injury
5] Acute Respiratory distress syndrome
6] Thromboembolism

• Educate patients and provide written sick day rules
• Provide sticks for urine ketone testing and educate on management of
ketonuria
• Warn about potential insulin ineffectiveness e.g from expired insulin
Prevention of DKA

Sick day rules:
• Continue your insulin when you are not feeling well
• If vomiting check glucose levels more frequently
• Take small amounts of carbohydrates in liquid form with short-acting insulin
• Seek help early if you continue to feel unwell
Prevention of DKA

Hyperosmolar Hyperglycaemic State
( H H S )

HHS – incidence and features
 0.5% of primary diabetes hospital admissions
 ~15% mortality rate

• This condition , in which severe hyperglycaemia
develops without significant ketosis.
• Is a metabolic emergency characteristic of
uncontrolled type 2 DM
• Infection ,myocardial infaraction , stroke or recent
surgery is the precipitating factors.

Pathogenesis of HHS
• Insulin enough to suppress ketogenesis but not to prevent hyperglycemia
• 20% of cases of HHS occur in those not previously known diabetic
•Delayed recognition of hyperglycemic symptoms + restricted water intake in
elderly leads to severe dehydration

Pathogenesis of HHS
Severe hyperglycemia
Osmotic diuresis
Renal loss of water in excess of sodium
Hypernatremia
Increased osmolality

Symptoms and Physical Signs
Symptoms Physical Signs
Polyuria Dehydration
Polydipsia
Tachycardia
Hypotension
Altered Conciousness

Hypovolaemia
Marked hyperglycaemia (30mmol/L or more) (540mg/dl or more)
No significant ketonaemia
or acidosis
<3mmol/L) or acidosis
pH >7.3
Bicarbonate >15mmo/L
Osmolality
Calculated osmolality
≥ 320mmol/kg
(2 Na + glucose + urea)
HHS Diagnostic Criteria

HHS – causes or triggers
Booth 2001
Incidence
Infection 40-60%
New-onset diabetes
Myocardial Infarction / Stroke
33%
Acute illness 10-15%
Medicines, steroids <10%
Insulin omission 5-15%

73
Investigations
Immediate for diagnosis:
• Plasma glucose
• Sodium with calculation of plasma osmolality
• Potassium and urea
• Venous pH/ bicarbonate (or arterial blood gas if indicated)
• Urine ketones
Urgent for assessment and treatment:
• Complete blood count
• Creatinine
• Midsteram urine
• HbA1c
• Blood film for malaria (if indicated)
• ECG
• C X ray

• Normalize the Osmolality
• Replace Fluid and electrolyte losses
• Normalize blood glucose
• Treat the underlying cause
• Prevent arterial or venous thrombosis
• Prevent other potential complications, e’g cerebral oedema /
central pontine myelinosis
Goal of treament of HHS

• Osmolality >350 mOsmol/kg
• Sodium >160 mmol/L
• Glasgow coma scale <10
• Systolic BP<90 mmHg
Indications for admission to ICU

• Reduce plasma
osmolality by 3-8
mOsmol/kg/hour
• Reduce plasma glucose
by 55-90 mg/dL/hour
Aims of treatment in HHS
• Target plasma osmolality:
<315 mOsmol/kg
• Target plasma glucose:
180-250 mg/dL

Monitoring
Hourly:
• Pulse
• BP
• RR
• Fluid input/output
• Capillary glucose
Four Hourly:
• Plasma glucose and sodium (with calculation of plasma osmolality)
• Potassium

IV fluids
• 0.9% normal saline is the fluid of choice
• When glucose reaches 250 mg/dL, change to 10% dextrose at a rate of 125 ml/hour
• The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours

IV fluids
1st
2nd
3rd
4th
5th
Suggested guide for rate of IV saline infusion for most patients with HHS

IV fluids
• If systolic BP <90 mmHg, give 500 ml saline over 15 minutes
• Repeat if SBP still <90 mmHg
• In patients with cardiac or renal impairment, adjust rate accordingly
• A urinary catheter may be needed to monitor urine output

Potassium Replacement
If plasma potassium result available quickly on admission, follow table below:
Serum potassium Potassium chloride/litre fluid
> 5.5 mmol/L Give saline with no added KCl
3.3 - 5.5 mmol/L Add KCl 20 mmol to each 500 ml bag of
saline
<3.3 mmol/L Add KCl 20 mmol to each 500 ml bag of
saline and:
- consider increasing rate of infusion if
fluid balance allows
- withhold insulin until potassium 3.3

Potassium Replacement
If plasma potassium result not available on admission:
• The first 2 bags of 500 ml saline should be without added potassium
• When potassium result known, follow previous table

Insulin Therapy
• Fluid replacement alone (without insulin) will lower plasma glucose
• Start insulin only if:
oRate of fall plasma glucose is less than 55 mg/dL/hour
oUrinary ketones ≥++ (i.e mixed DKA and HHS)
• Aim for reduction in plasma glucose of 55-90 mg/dL/hour
• Target plasma glucose is 180-250 mg/dL

Insulin Therapy
If syringe infusion pump available:
• Add 50 units of soluble human insulin (e.g actrapid) to 50 ml normal saline, this
gives a concentration of 1 unit/ml
• This should be infused into a separate IV line and the solution should be changed
every 6 hours
• Infuse at a fixed rate of 0.05 unit/kg/hour, based on estimating patient’s weight
(e.g 4 units/hour in an 80 kg person)

Resolution of HHS
Stop insulin (IV) when:
• The patient is fully conscious
• Well-hydrated
• Eating and drinking
• Plasma osmolality <315 mOsmol/kg

• If previously on insulin: restart usual insulin regime
• If previously on diet/oral hypoglycemic drugs: restart if clinically well and
stable
• If newly diagnosed diabetes: decide on appropriate treatment (diet, OHAs
or insulin) depending on clinical condition and HbA1c
• Educate patient to reduce risk of recurrence of HHS
Management of the recovery
Period From HHS

 Treat the underlying cause
 Anticoagulation
Because of increase risk of arterial and venous thromboembolism , all patients
should received prophylactic low molecular wt heparin, for the full duration of
admission unless contraindicated.
 Prevent foot ulceration
This patient are at high risk of pressure ulceration , so an intial foot assessement
should be done.

HHS – complications
Complication Prevention
Hypoglycaemia Prevent by adding glucose infusion
when glucose <14mmol/L (250
mg/dL)
Hypokalaemia Early potassium replacement and
monitoring
Fluid overload Careful clinical monitoring and
central line as needed
Cerebral oedema

DKA or HHS Vs DKA HHS
Age Any old
Diabetes type T1 DM (less common in T2 DM) T2 DM
Period of development Hours Days
Glucose ++ ( usually > 350 mg/dl ) ++++ ( usually > 540 mg/dl )
Hyperosmolality > 320 mOsmole/kg
Bicarbonate < 15 > 15
pH < 7.3 > 7.3
Urinary ketones > ++ +
Water deficit (L) 4 ---- 10 L 8 ---- 15

Message
 Educate the patient about diabetes
 Nutrition Advice about the diabetic diet
 Exercise program 150 min / week
 Regular follow up and investigation
 Compliance with the medication
 Educate about insulin injection

• Identify and treat the underlying cause
• Can be prevented by
 Better public awareness
 Improved access to medical care
 Improved education in treating
hyperglycaemia during illness
 Emergency communication with
healthcare provider .
DKA and HHS – prevention key

B) Chronic complications of Diabetes

Chronic complications of DM
1) Microvascular complications :
a) Diabetic retinopathy (DR)
b) Diabetic nephropathy
c) Diabetic neuropathy
d) Autonomic neuropathy
e) The diabetic foot

2) Macrovascular complications :
Vascular diseases
a) Cardiovascular diseases e.g Myocardial infarction
b) Cerebrovascular diseases
c) Peripheral vascular diseases

1) Microvascular complications :
Diabetic retinopathy , nephropathy and neuropathy tend to manifest 10 years after
diagnosis in young patients but may present earlier in older patients, probably
because these individuals have had unrecognized diabetes for months or even years
prior to diagnosis.

Diabetic eye disease
Diabetes is still the most common cause of blindness in under- 65-year-olds.
It affects the eye in a variety of ways:
• Cataract
is denaturation of the protein and other components of the lens of the eye,
which renders it opaque.
• Diabetic retinopathy
is damage to the retina and iris caused by diabetes, which can lead to
blindness.
• External ocular palsies
most commonly affect the sixth and the third nerves.
. Third nerve palsy is not associated with pain.
 These nerve palsies usually recover spontaneously within a period of 3–6
months.

 Damage to the blood vessels in the retina, causing bleeding, leakage, and potentially
blindness.
 Early symptoms: blurry vision , floaters.
 Late symptoms: macular edema, retinal detachment.

 Risk factors for Diabetic Retinopathy
- Uncontrolled Diabetes Mellitus
- Uncontrolled Hypertension
- Uncontrolled Hyperlipidaemia
- Smoking
- Age
- Duration of Diabetes
 Screening of Diabetic Retinopathy
- Type 1 Diabetes within 5 years after the onset of diabetes.
- Type 2 Diabetes at the time of the diabetes diagnosis

Diabetic retinopathy treatment
• Early detection and treatment of diabetic retinopathy can significantly improve
the prognosis.
• Strict glycemic control: Lowering blood sugar levels is crucial for slowing
progression.
• Laser therapy: Targets and seals leaking blood vessels or abnormal new vessels.
• Anti-VEGF medications: Injections that inhibit vascular endothelial growth
factor (VEGF), promoting abnormal blood vessel growth.
• Vitrectomy: Surgical removal of vitreous hemorrhage in severe cases.

The Diabetic kidney
 The kidney may be damaged by diabetes in three main ways:
1) Glomerular damage
2) Ischaemia resulting from hypertrophy of afferent and efferent arterioles
3) Ascending infection.
 Glomerular endothelial dysfunction and basement membrane thickening
impair filtration , leading to proteinuria, waste buildup, and eventually kidney failure.
 Microalbuminuria is a predictive marker of progression to nephropathy in type 1
diabetes, and of increased cardiovascular risk in type 2 diabetes.

Diabetic Nephropathy Classification
• Stage 1: Microalbuminuria (eGFR > 90 mL/min/1.73 m²)
• Elevated albumin in the urine, early sign of kidney damage.
• Often asymptomatic, requiring regular urine albumin-to-creatinine ratio (UACR) testing for
detection.
• Stage 2: Mildly Decreased eGFR (60-89 mL/min/1.73 m²)
• Early decline in kidney function, with elevated urine albumin-creatinine ratio (UACR) and
mild hypertension.
• Increased risk of progression to advanced stages if not managed effectively.

• Stage 3: Moderate Kidney Disease (45-59 mL/min/1.73 m² or 30-44 mL/min/1.73 m²)
• Further decline in GFR, with UACR significantly elevated and symptoms like fatigue and
anemia potentially emerging.
• Stage 4: Severe Kidney Disease (15-29 mL/min/1.73 m²)
• GFR significantly reduced, indicating substantial kidney damage.
• Proteinuria (excessive protein in urine) and electrolyte imbalances become evident.
• Stage 5: Kidney Failure (End-Stage Renal Disease - ESRD)
• GFR below 15 mL/min/1.73 m², requiring dialysis or kidney transplantation for survival.

Diabetic Nephropathy Diagnosis
• Urinalysis: Checks for protein and albumin in the urine (indicating kidney damage).
Assessment of albuminuria by measuring early morning spot urine for Urine Albumin
Creatinine Ratio ( Urine ACR ).
To confirm albuminuria collect (3 samples) at least 3 – 6 months interval and (2 samples)
from 3 must be abnormal
Normal ACR < 30 mg/g
Microalbuminuria 30 -300 mg /g
Macroalbuminuria > 300
• Blood tests: Assess kidney function through creatinine and glomerular filtration rate (GFR)
measurement.
• Kidney ultrasound: Visualizes the kidneys and identifies structural abnormalities(glomerular
sclerosis)

Diabetic Nephropathy Treatment
• Blood pressure control: Crucial for slowing kidney damage.
• Strict glycemic control: Essential for protecting kidney function.
• ACE inhibitors or ARBs: Medications to lower blood pressure and protein in
the urine.
• SGLT2 Inhibitor ( Sodium glucose transport 2 inhibitor) e.g Forxiga if
eGFR > 30 mL/min
• Dietary changes: Low-protein diet to reduce workload on the kidneys.
• Dialysis or kidney transplantation: May be necessary in advanced stages of
kidney failure.

Diabetic Neuropathy
 Hyperglycaemia leads to increased formation of sorbitol and fructose in Schwann cells,
accumulation of these sugars may disrupt function and structure of the nerve.
 The earliest functional change in diabetic nerves is delayed nerve conduction velocity; the
earliest histological change is segmental demyelination, caused by damage to Schwann cells.
 Hyperglycemia damages both sensory and autonomic nerves, causing numbness, pain, and
impaired organ function like digestion and bladder control.

The Following Varieties of Neuropathy Occur
1) Symmetrical, mainly sensory polyneuropathy (distal)
2) Acute painful neuropathy
3) Mononeuropathy and mononeuritis multiplex
– cranial nerve lesions
– isolated peripheral nerve lesions
4) Diabetic amyotrophy (asymmetrical motor diabetic neuropathy)
5) Autonomic neuropathy.

Autonomic neuropathy ;
1) Gustatary sweating
2) Cardiac denervation ( resting tachycardia.. Orthostatic hypotension)
3) Postural hypotension
4) Gastroparesis ( constipation .. Delayed gastric emptying )
5) Autonomic Diarrheae
6) Neuropathic bladder (Atonic bladder)
7) Erectile dysfuction

Diabetic peripheral Neuropathy (PND)
 Symptoms
- Feeling tingling and numbness peripherals
 Assessment
- 10 g monofilament
- Tuning fork 128 test ( vibration test )
- Pinprick and temperature
 Treatment of PDN
- Duloxetin ( SSRI )
- Pregabalin
- Gabapentin
- Anticonvulsant (Carbamazine )
- Antidepressant ( Amitryptyline )

The Diabetic Foot
 A total of 10–15% of diabetic patients develop foot ulcers at some stage in their
lives.
 Diabetic foot problems are responsible for nearly 50% of all diabetes-related hospital
admissions.
 Many diabetic limb amputations could be delayed or prevented by more effective
patient education and medical supervision.
 Ischaemia, infection and neuropathy combine to produce tissue necrosis.

 The examination should include the following :
- Inspection of the skin
- Assessment of foot deformities
- Neurological assessment by 10 g monofilament
- Pinprick … temperature
- Vibration
- Vascular assessment including pulse in the legs and feet.
 Imaging :
- X- ray foot bones
- MRI foot to detect abscess
- CT Angiography
- Doppler u/s lower limb -

A:Diabetic ulcer / B: gangrene
A B

2) Macrovascular complications :
Vascular diseases
a) Cardiovascular diseases e.g Myocardial infarction
b) Cerebrovascular diseases
c) Peripheral vascular diseases
 Chronic hyperglycemia promotes atherosclerosis, the buildup of fatty plaques in arteries.
This narrows blood vessels, decreases blood flow, and increases the risk of blood clots.

Diabetic risk factors for macrovascular complications
• Duration
• Increasing age
• Systolic hypertension
• Hyperinsulinaemia due to insulin resistance associated with obesity and
the metabolic syndrome
• Hyperlipidaemia, particularly hypertriglyceridaemia/ low high-density
lipoprotein (HDL)
• Proteinuria (including microalbuminuria)
• Smoking

Coronary Artery Disease
• Build-up of plaque in the coronary arteries leading to narrowed blood flow
and heart attacks or heart failure.
• Risk factors: high blood pressure, cholesterol, smoking.
• Image: Angiography showing a blocked coronary artery.

Peripheral Artery Disease
• Narrowing of arteries in the legs leading to pain, numbness, and gangrene.
• Risk factors: smoking, obesity, high cholesterol.
• Image: Leg with discoloration and ulcers due to peripheral artery disease.

Stroke
• Sudden interruption of blood flow to the brain causing brain damage.
• Types: ischemic (clot) and hemorrhagic (bleeding).
• Image: Brain scan showing a hemorrhagic/ischaemic stroke.

Management
• Heart Disease and Stroke:
• Maintain good blood sugar control through medication, diet, and
exercise.
• Manage blood pressure and cholesterol levels through medication
and lifestyle changes.
• Maintain a healthy weight.
• Don't smoke.
• Get regular checkups and screenings for heart disease and stroke.

Feature Ischaemia Neuropathy
Symptoms Claudication
Rest pain
Usually painless
Sometimes painful neuropathy
Inspection Trophic changes High arch
Clawing of toes
No trophic changes
Palpation Cold
Pulseless
Warm
Bounding pulses
Ulceration Painful
Heels and toes
Painless
Plantar

Necrobiosis lipodica dibeticorum

References
• American Association of Diabetes: Diabetes Care in the Hospital: Standards of Medical Care in Diabetes—2024
https://doi.org/10.2337/dc22-S016
• Up to Date
• Oxford textbook of Endocrionolgy and Diabetes 4th
edition
• Williams textbook of endocrinology

Acute and Chronic Complication of Diabetes.pptx

Acute and Chronic Complication of Diabetes.pptx

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