COMPLICATIONS OF DM

By

.Hany Ahmed Khalil, MD

Lecturer of Internal Medicine

I. Acute complications .

II. Chronic complications .

We classify it into 4parts
1.Hypoglycemia
2.Diabetic ketoacidosis
3.Hyperglycemic hyperosmolar state (HHS)
(non ketotic hyperosmolar diabetic coma)
4.Lactic acidosis
 ACUTE COMPLICATIONS

1. Hypoglycemia.

2. Diabetic ketoacidosis (DKA).

3. Hyperglycemic hyperosmolar state (HHS)

{ Non ketotic hyperosmolar diabetic coma}.

4. Lactic acidosis .
.HYPOGLYCEMIA

Hypoglycemia in non diabetics called spontaneous

hypoglycemia.
Causes :
 Insulinoma.
 Tumors (IGF-1).
 Drugs (NSAID).
 Hepatic &renal disease .
 Endocrine causes.
 Alcohol .
:CAUSES OF HYPOGLYCEMIA IN DIABETIC PATIENTS
More frequent in insulin treated patients
1. Missed ;delayed or infrequent meals.
2. Unusual exercise.
3. Poorly designed insulin therapy.
4. Impaired awareness of hypoglycemia.
5. Gastroparesis due to autonomic neuropathy.
6. Unrecognised other endocrine disease e.g. addison’s
7. Malabsorption.
8. Factitious.(insulin, oral ttt abuse).
9. Lipodystrophy
10. Alcohol.
RISK FACTORS FOR SEVERE HYPOGLYCEMIA
 Strict glycemic control. loock (accord trial)
 Impaired awareness of hypoglycemia .
 Age (very young ,old age ).
 Long duration of diabetes.
 Sleep .
 Negative C peptide (complete insulin deficiency ).
 History of previous severe hypoglycemia .
 Renal impairment.
 Genetic.
HYPOGLYCEMIA
SYMPYOMS:
A-AUTONOMIC:
Sweating; hunger; anxiety; pounding heart

B-NEUROGLYCOPENIC:
Confusion; drowsiness; inability to concentrate;
speech difficulty ; incoordination, irritability.
C-NON SPECIFIC:
Headache; nausea; tiredness
HYPOGLYCEMIA

MORBIDITY OF SEVERE HYPOGLYCEMIA:

A-CNS:
CONVULSIONS.
IMPAIRED COGNITIVE FUNCTIONS.
VASCULAR EVENTS; COMA.
B-HEART
ARRHYTHMIAS; MYOCARDIAL ISCHEMIA.

C-EYE;
VITRIOUS hge.

D- OTHERS
HYPOTHERMIA;INCREASED ACCIDENTS …
HYPOGLYCEMIA: MANAGEMENT

 Simple oral cho if patient is conscious and early

recognized.

 I.V 30-50ml of 50%dextrose.(followed by 0.9 saline flush).

 Glucagon i.m 1 mg in insulin induced hypoglycemia.

 In suspected case of cerebral edema give mannitol;

dexamethazone and high dose of O2.

 After recovery; try to identify the cause and treat it.

DIABETIC KETOACIDOSIS
A major medical emergency with mortality rate of 5-10%
Principally occur in type 1 DM but could occur in type 2
DM under severe stressful conditions
Cardinal biochemical features are: hyperglycemia;
hyperketonemia; and metabolic acidosis.
Clinical features:
A-SYMPTOMS: Polyuria; thirst; weakness, weight loss;
nausea and vomiting; leg cramps; blurred vision;
abdominal pain ”children”
B-SIGNS: Dehydration; hypotension; tachycardia; air
hunger; smell of acetone; hypothermia; confusion;
drowsiness and coma”10%.”
COMPLICATIONS OF DKA

o CEREBRAL EDEMA.

o ACUTE RESPIRATORY DISTRESS SYNDROME.

o THROMBOEMBOLISM.(DVT).

o DIC.

o ACUTE CIRCULATORY FAILURE.

o COMPLICATIONS OF THERAPY.(eg. K+↑↓ ).

MANAGEMENT OF DKA

 HOSPITALIZATION.
 LAB MONITORING: Plasma glucose; urea;
electrolytes; PH and bicarbonate ;ketone bodies in
blood and urine.
 1-INSULIN:
Recently, inhaled insulin was used for management of DKA
in a patient with subcutaneous insulin resistance syndrome.
However, IV continuous infusion with regular insulin
remains the mainstay of treatment due to its short half-life
and easy titration in comparison to other modes of
administration.
Treatment algorithms recommended the administration of an
initial intravenous dose of regular insulin (0.1 unit/kg)
followed by infusion of (0.1 unit/kg/h). Other studies
showed that an hourly insulin infusion of (0.14 units/kg
body wt) would be sufficient without a bolus dose.
Monitor glucose (every 1 to 2 h) and expect decrease
of 50 to 75 mg/dL/h. If the level did not drop, then
infusion rate should be increased or bolus another
dose of 0.14 unit/kg.
When the plasma glucose reaches 200 mg/dL, the
rate of insulin infusion should be decreased to
0.02–0.05 unit/kg/h. Continue close monitoring
glucose to maintain glucose level at 150–200
mg/dL.
 2-FLUID REPLACEMENT:

Since DKA patients experience fluid loss of approximately

6–9 L, the goal of fluid resuscitation aims to replete that
volume within 24–36 h with 50% of resuscitation fluid
administered within first 8–12 h of presentation.
Current DKA guidelines recommend initiating volume
repletion with isotonic saline (0.9% NaCl) at 15–20
mL/kg/h followed by hypotonic saline solution (0.45%
saline) at a rate of 4–14 mL/kg/h then re-evaluate.
Traditionally, hyperglycemia is corrected faster than
ketoacidosis (6 and 12 h, respectively). Hence, when
glucose levels fall below 200–250 mg/dL, intravenous
fluids should be switched to dextrose-containing 0.45%
NaCl solution to allow continued insulin administration
until ketonemia and avoid hypoglycemia.
 3-POTASSIUM: (3.5 :5 mmol/L))
Despite total-body potassium depletion, patients with
hyperglycemic crises can present with mild hyperkalemia that
could be attributed to reduced glomerular filtration rate
and/or extracellular shift of potassium.
Hypokalemia can cause life-threatening arrhythmias and
respiratory muscle weakness. In such cases, potassium
replacement should begin with fluid therapy, and insulin
treatment should be delayed until potassium concentration
is restored to >3.3 mEq/L.
Generally, administration of 20–30 mEq potassium in each
liter of infusion fluid is sufficient to maintain a serum
potassium concentration within the normal range of 4–5
 Bicarbonate
In severely acidotic pt; PH < 7 infusion of 300 ml over 30
min. Complete correction of acidosis should not be
attempted.
In most cases correction occurs spontaneously with
correction of blood glucose and K deficits .
MANAGEMENT OF DKA
5- ANTIBIOTIC:
If infection demonstrated or even suspected.

6-ADDITIONAL PROCEDURES:
 Urinary catheterization.
 Nasogastric tube.
 Central venous line.
 Plasma expanders in profound low BP.
 Mannitol, O2 in cerebral edema.
Hyperglycemic hyperosmolar state (HHS)
(non ketotic hyperosmolar diabetic coma)

HHS is a clinical condition that arises from a complication

of diabetes mellitus. Type 2 diabetes accounts for about
90% to 95% of diabetes cases. It is most commonly seen
in patients with obesity.
The mortality rate in HHS can be as high as 20% which is
higher than the mortality seen in diabetic ketoacidosis.
Etiology
Approximately 50% to 60% of HHS is attributable to an
infectious etiology.
Some medications for the treatment of other ailments and
conditions in elderly patients with type 2 diabetes can
trigger HHS. Examples of such medications are thiazide
diuretics, beta-blockers, glucocorticoids, and some atypical
antipsychotics.
A cardiovascular insult like stroke, angina pectoris, and
myocardial infarction can also trigger a stress response.
 CLINICAL PRESENTATION
Polyuria Tachycardia
Polydipsia Orthostatic hypotension
Dehydration Weak and thready pulse
Weakness, malaise, and Decreased urine output
lethargy
Focal neurological deficit
Disturbance in visual acuity
Delirium
Coma
Treatment
fluid
Aggressive hydration with isotonic fluid with electrolyte
replacement is the standard practice in the management of
HHS. An initial fluid bolus of 15 to 20 ml/kg/h or greater
is indicated to expand the extracellular volume quickly in
the first hour.
This amounts to about 1-1.5 L in an average-sized person. (In
patients with contraindications to rapid fluid resuscitation
[ie, cardiac or renal disease], slower rates are indicated.) A
greater rate of fluid resuscitation is needed in patients with
severe volume depletion but should not exceed 50 mL/kg
in the first 4 hours.
When the blood glucose concentration, initially checked
hourly, reaches 250 mg/dL, change the infusion to 5%
dextrose in 0.45-0.7% normal saline. This helps to prevent
a precipitous fall in glucose, which may be associated with
cerebral edema.
Potassium
The serum potassium in HHS is usually high, but the total
body potassium is low as a result of the extracellular shift
from lack of insulin. Potassium replacement should be
started when the serum potassium is between 4 to 4.5
mmol/L.
Insulin
Care should be taken to avoid starting insulin drip in the
initial stage of treatment as this might cause a rapid drop in
serum glucose levels leading to cerebral edema.
• If hypokalemia (K < 3.3mEq/L) has been excluded, an IV
bolus of regular insulin of 0.10 U/kg/h should be
administered.
• Begin a continuous insulin infusion of 0.1 U/kg/h.
• Monitor blood glucose by means of bedside testing every
hour; if glucose levels are stable for 3 hours, decrease the
frequency of testing to every 2 hours.
 If plasma glucose levels do not achieve a reduction of 50
mg/dL in the first hour, check volume status. If volume
status is normal, it is okay to double insulin infusion every
hour until a drop in glucose of 50-75 mg/dL is obtained.
 Set the target blood glucose level at 300 mg/dL; this target
level may be adjusted downward after the patient is
stabilized.
 Once blood glucose concentration reaches 300 mg/dL,
decrease the insulin infusion rate by 0.5-1.0 U/h. Add
dextrose to the IV fluids.
Do not discontinue the insulin drip. Continue IV insulin at a
goal glucose level of 250-300 mg/dL until the patient
becomes more alert and hyperosmolarity has resolved.

Treatment of other risk factors

Like infection
LACTIC ACIDOSIS
 Occurs in type 2 DM pts receiving biguanides with hepatic
;renal problems ;hypoxemia and shock.

 Patient is very ill ;acidotic breathing but not dehydrated.

 Diagnosis by increase lactic acid and decrease bicarbonate.

 Treatment by iv sodium bicarbonate + insulin

 Mortality rate>50%.
 CHRONIC COMPLICATIONS
(LONG TERM COMPLICATIONS)
Microvascular complications :
 Diabetic neuropathy
 Diabetic nephropathy
 Diabetic retinopathy
 Diabetic foot disease.
Macrovascular complications:
 Coronary
 Cerebral
 Peripheral
LONG TERM COMPLICATIONS OF DM
PATHOGENESIS:
A-BIOCHEMICAL CONSEQUENCES OF HYPERGLYCEMIA
 Non enzymatic glycation ( ↑ glycated end products).
 Oxidative reduction stress (reactive O2 species ).
 Increased polyol pathway activity.
 Myo-inositol depletion.

B-FUNCTIONAL ABNORMALITIES
 Increased capillary permeability.
 Microvascular hypertension.
 Endothelial dysfunction& proliferation.
 Hemorrheological and coagulation abnormalities .
 The hallmark of diabetic microangiopathy is capillary

BM thickening and increased vascular permeability.

 Macrovascular complications “coronary; cerebral and

peripheral” are the same that occur in non-diabetic pts

but more extensive and occur early in life

DIABETIC NEUROPATHY
Early and common complication affecting 30% of all diabetics
Its development related to long duration of DM and poor glycemic control
CLASSIFICATION
A-SOMATIC B-AUTONOMIC
1- POLYNEUROPATHY

 Symmetrical: 1- Cardiovascular

mainly sensory and distal

2- Gastrointestinal
 Asymmetrical
mainly motor and proximal 3- Genitourinary

4- Vasomotor

2- MONONEUROPATHY
5- Pupillary
CLINICAL FEATURES OF DIABETIC NEUROPATHY
1-SYMMETRICAL SESORY POLYNEUROPATHY:
-FREQUENTLY ASYMPTIMATIC; PARATHESIA ARE COMMON
-symmetrical deminished vibration distally;decreased tendon
reflexes; glove&stock hypothesia
-in severe cases; muscle wasting; clow toes; callous skin and foot
ulcers.
2-ASYMMETRICAL MOTOR NEUROPATHY
“DIABETIC AMYOTROPHY”

-severe progressive weakness and wasting of proximal muscles of

L.L. accompanied by severe pain on the anterior aspect of the legs;
parathesia;weight loss ;the condition may involve acute infarction of
LMN of lumbosacral plexuses.

Recovery usually occurs within one year

3-MONONEUROPATHY:
-affect single peripheral or cranial nerve
-mostly rapid and severe
-cranial nerves :3;4;7
-peripheral nerves: femoral;and sciatic .less commonly median and
lateral popliteal
4-AUTONOMIC NEUROPATHY
-CVS: postural hypotension;resting tachycardia; fixed heart
rate;sudden cardiac arrest
-GIT: dysphagia;gastroparesis;nocturnal diarrhea ;constipation
-GENITOURINARY :difficult micturation;incontinence;UTI;impotence;
retrograde ejaculation.
-VASOMOTOR :feet coldness;dependent edema;bullous formation
-PUPILLARY: decreased pupil size;resistance to
mydriatics;abnormal reaction to light .
MANAGEMENT OF DIABETIC NEUROPATHY
1-Strict glycemic control.
2-Tricyclic antidepressants.& SSRI
3-Anticonvulsants.
4-Support stockings; fludrocortisone and adrenoreceptor
agonists for postural hypotension.
5-Dopamine agonists for gastroparesis.
6-Loperamide and broad spectrum antibiotics for diarrhea.
7-Stimulant laxative for constipation.
8-Anticholinergic drugs for excessive sweating.
9-Sildenafil & psychologic support ;papaverine;
prostaglandine for impotence.
DIABETIC KIDNEY DISEASE
Important cause of end stage renal disease .
RISK FACTORS :
1-Poor control of DM
2-Long duration of DM
3-Presence of other microvascular complications.
4-Racial groups
5-Pre-existing hypertension
6-Family history of hypertension or nephropathy
PATHOLOGICALLY:
Thickening of GBM followed by increased mesangeal matrix then
nodular sclerosis and progressive loss of glomeruli.
Microalbuminuria is an important indicator for developing overt
diabetic nephropathy especially in type 1 DM. (albumin /cr
ratio.)

o Males ACR 2.5 -30 mg/ mmol creatinine

o Females ACR 3.5 -30 mg /mmol creatinine

 Microalbuminuria present if ACR > 30 mg /mmol.

 ACR > 300 mg /mmol creatinine → overt nephropathy,

(Macroalbuminuria).
CLINICAL FEATURES:
1-Long history of DM especially type 1. after 5 yrs
2-Nephrotic stage :proteinuria and edema state.
3-Hypertension.
4-Progressive renal impairment and ESRD .
PREVENTION & MANAGEMENT:
1-Good control of DM.
2-Good control of B P <130/80.
3-ACE inhibitors.
4-Renal replacement therapy .
 DIABETIC RETINOPATHY
The most common cause of blindness in adults in developed countries
Retinal photocoagulation is effective treatment provided given at early
stage.
CLINICAL FEATURES:

1-MICROANEURYSMS: the earliest clinical signs; appear as minute

discrete circular red spots.

2-Haemorrhages: occur in the deeper layers of retina as dots and

blots ;also flame- shaped haemorrhage can occur in hypertensive
diabetics.

3-Hard exudates: is characteristic for diabetic retinopathy; variable in

size; in the perivascular area; result from retinal capillary leakage .
.,CLINICAL FEATURES: CONT

4-SOFT EXUDATES:COTTON-WOOL SPOTS;similar to those seen in

hypertensive retinopathy; represent retinal ischemia

5-INTRA-RETINAL MICROVASCULAR ABNORMALITIS (IRMA) :dilated

tortuous capillaries.

6-NEUVASCULARIZATION

7-VENOUS CHANGES: dilatation; bleeding and increased tortuosity

8-Pre-retinal haemorrhage

9-Vitrous haemorrhage

10-Fibrosis & RD.

;CLASSIFICATION:

1-Non-proliferative “background”:
peripheral microaneurysms ;venous dilatation;small hgs&
exudates.

2-Preproliferative reinopathy/ or maculopathy:

venous bleeding sheets of microaneurysms; multiple
hges & exudates; macular edema; perimacular exudates.

3-Proliferative retinopathy /maculopathy:

pre-retinal hge; neuvascularization; fibrosis;exudative
maculopathy .
 PREVENTION:
1-Glycemic control
2-Screaning
3-Control of other risk factors
 TREATMENT:
Retinal photocoagulation
 OTHER OPHTHALMIC COMPLICATIONS :
 Errors of refraction.
 Cataract.
 Rubiosis iridis & secondary glucoma.
 External ocular palsies.
DIABETIC FOOT
Tissue necrosis in the feet that frequently requires
hospital admission and may be ends with amputation at
various levels.
ETIOLOGY:
Trauma “often trivial” in presence of neuropathy and /or
peripheral vascular disease with infection occurring as
secondary event following ulcerations.
CLINICAL FEATURES:

1-Neuropathy:none; parathesia;pain

2-Ischemia: none;claudication; rest pain

3-Structural :ulcers;sepsis; abscess; osteomyelitis; digital

gangrene ;charcot joint .(nueropathic joint)
DIABETIC FOOT: MANAGEMENT
1-EDUCATION : learning principles of diabetic foot care.
2-CONTROL OF INFECTION:
-Early antibiotic treatment
-Debridement of non viable tissues and excision of infected bone if
osteomylitis occurs.
-good drainage of pus pockets.
3-TREATMENT OF ISCHEMIA:
-CLINICAL&DOPPLER ASSESSMENT.
-ANGIOPLASTY OR BYPASS SURGERY.
4-DEAL WITH ABNORMAL PRESSURE.
5-WOUND DRESSING.
6-STRICT GLYCEMIC CONTROL.
7-STRICT CONTROL OF OTHER RISK FACTORS.
DIABETES &INFECTIONS
Diabetic pts are more susceptible to infections than general populations due to
depressed phagocytic and chemotactic functions of leucocytes by hyperglycemia

Common infections:
1-Skin:staph. ;mucocutaneous candidiasis
2-Urinary tract :pyelonephritis; perinephric abscess
3-Respiratory tract: staph.; pneumococcal and gram –ve pneumonia &pulmonary
TB.
4-GIT:chronic periodonitis ;rectal& ischiorectal abscess.

Impact on management:
1-Decrease glycemic control.
2-Increase susceptibility to DKA.
3-DO NOT OMIT THERAPY.
4-Insulin dose increase by 25%.
5-Shift tablets to insulin.
6-Vaccination .
THANK YOU