Musculoskeletal manifestations of diabetes mellitus

Musculoskeletal
Manifestations
Of
Diabetes Mellitus
Dr. Fathi Neana, MD
Chief of Orthopaedics
Dr. Fakhry & Dr. A. Al-Garzaie Hospital
August,15 - 2018

َ‫ين‬ِ‫ف‬ ِ‫ر‬ْ‫س‬ُ‫م‬ْ‫ل‬‫ا‬ ُّ‫ب‬ ِ‫ح‬ُ‫ي‬ َ‫َل‬ ُ‫ه‬َّ‫ن‬ِ‫إ‬ ۚ ‫وا‬ُ‫ف‬ ِ‫ر‬ْ‫س‬ُ‫ت‬ َ‫َل‬َ‫و‬ ‫وا‬ُ‫ب‬َ‫ْر‬‫ش‬‫ا‬َ‫و‬ ‫وا‬ُ‫ل‬ُ‫ك‬َ‫و‬(31)‫اَلعراف‬ ‫سورة‬
Eat and drink, and do not waste. He does not love the wasteful. (31) AL-ARAF

New Lifestyle diseases
Non-communicable diseases (NCDs)
• Obesity
• Metabolic syndrome
• Coronary artery disease
• Diabetes type 2
• Hypertension
• Arteriosclerosis
• Stroke
• Cancer
• Depression - anxiety
• Arthritis
• Osteomalacia
• Osteoporosis
• Swimmer's ear – loss of hearing
• Ch. obstructive pulmonary disease
• Liver Cirrhosis
• Nephritis
• Etc, etc, etc…
Emerged as bigger killers than infectious or hereditary ones.
The leading cause of death in the world.
63% of all annual deaths.
> 38 million people are killed /year.
1- Cardiovascular diseases (17.5 million)
Complications of hypertension (9.4 million)
2- Cancers (8.2 million)
3- Respiratory diseases (4 million)
5- Diabetes (1.5 million)
These 4 diseases account for 80 % of all NCDs deaths (> 38 million)
4- USA’s 4th Leading Cause of Death – Pharma’s Drugs
Posted on June 25, 2012 by Child Health Safety
Causes:
• Stress-Depression
• Diet
• Sleep-awake
• Lack of Exercise
• Sun avoidance
• Wireless WiFi devices
• Leaky gut syndrome
• Other pollutants
Including Medicines

The Root cause and Culprit behind
Chronic Diseases, Cancer and Aging
1- A state of chronic low grade
inflammation
Dr. Richard K. Bernstein
Diabetes & Inflammation—the Vicious Cycle
(Hyperglycemia – Omega 6 - Obesity) - Leukotriene B(4) (LTB(4)
Lindsay Christensen
Lindsay Christensen is a health writer and researcher with her B.S. in
Biomedical Science and an Emphasis in Nutrition
(Pathogens, unhealthy diet, lack of exercise).
2- Mitochondrial dysfunction
(not the genetic make up)
Dr. Ron Rosedale
Breakthrough views on clinical metabolic biochemistry
1- Harmful Effects of too much Sugar
->> Insulin and leptin receptor resistance
->> Free radicals (ROS) 90% Mitochondria
2- Harmful Effects of too much Protein
->> Activation of the mTOR metabolic signaling pathway
3- Physical inactivity (lack of exercise)
4- Pollutants
5- Drugs causing mitochondrial toxicity
(Iatrogenic)
Mitochondrial dysfunction
Energy (ATP - ADP)
Leukotriene B(4) (LTB(4)
acts as a signal to relay
information from cell to
cell over long distances.

Obesity and Type 2 Diabetes
are high rocketed and reached an
epidemic after 1980
Since the low fat guidelines
1979
Obesity epidemic
Type 2 diabetes epidemic
(Insulin resistance 92%)
Increasing prevalence of type 2 diabetes (vertical bars) in the
United States between 1933 and 1997 with increasing per capita
percentage of carbohydrate intake from corn syrup (•) (14, 17)

Systemic disorders and musculoskeletal
manifestations are interrelated
Diagnosed systemic disorders
We expect musculoskeletal manifestations
Musculoskeletal manifestations
will guide us to the hidden systemic disorder
Countless sources of information
Plain X-rays can tell a lot
Even the lifestyle and food selection can help
in future expectations
Musculoskeletal manifestation of
systemic disorders

Is an integral part of its surrounding environment
(the body - the Host A B C)
Systemic disorders and musculoskeletal
manifestations are interrelated.
With Diagnosed systemic disorders ( Obesity – DM
etc..) we can expect the musculoskeletal
manifestations
With Musculoskeletal manifestations we can
expect a hidden or undiagnosed systemic
disorder.
There is a Countless sources of information
Like Plain X-rays which can tell a lot. Even the
lifestyle and food selection can help in future
expectations
The musculoskeletal
system

• Made up of Bones - Muscles – Tendons –
Cartilage – Ligaments - Nerves – Vessels
• The Bones of the skeleton are organs that
contain different tissues
• Bones tissues are dominated but it contain
other tissues
– Nervous tissue and nerves
– Blood tissue and vessels
– Cartilage in articular cartilages
– Epithelial tissue lining the blood
vessels
The musculoskeletal
system

• Bones tissue is one of the most remarkable
tissues of the human body
• Far from inert and lifeless, bones are living,
dynamic structures
• It is in a state of continuous turnover
(changeable)
• Noted for their strength and resiliency
during life, bones will remain after we are
long gone

Musculoskeletal system serve a wide variety of
diverse very important functions
5 major functions of skeleton:
1- Shape and support
2-Movement
3-Protection
4- Blood production
5- Storage
Functions of Muscles:
1- Movement
2- Maintenance of posture and muscle
tone
3- Heat production
4- protects bones and internal structures

Types of connective tissues:
1. Loose (areolar) connective tissue (delicate thin
layers between tissues; present in all mucous
membranes)
2. Adipose tissue (fat)
3. Dense connective tissue (tendons/ligaments)
4. Hyaline cartilage (nose/ends of long bones/ribs)
5. Elastic cartilage (outer ear/epiglottis)
6. Fibro cartilage (between vertebrae/knee joints/pubic
joint)
7. Bone (skeletal system)
8 Blood (blood stream)
Bone is a specialized connective tissue

Collagen fibers
A type of protein fiber found abundantly
throughout our body.
It provides strength and cushioning to
many different areas of the body, including
the skin.
Collagen fibers
Found in our various types of connective
tissue such as cartilage, tendons, bones,
and ligaments (musculoskeletal system)
Connective
tissue fibers
Purpose Components
Collagenous
fibers
Bind bones
and other
tissues to each
other
Alpha
polypeptide
chains
Elastic fibers
Allow organs
like arteries
and lungs to
recoil
Elastic micro
fibril and
elastin
Reticular
fibers
Form a
scaffolding for
other cells
Type III
collagen
Types of connective tissue fibers
Types of connective tissue fibers

Co-occurrence of several known
cardiovascular risk factors
Type 2 Diabetes
Central Obesity
Atherogenic dyslipidemia
Hypertension
The metabolic syndrome
Insulin Resistance syndrome - Syndrome X - Deadly quartet - Reaven’s syndrome
Definition
Abdominal obesity Plus two other
components (Elevated BP - Low HDL -
Elevated TG - Impaired fasting glucose)
These conditions are interrelated and
share underlying mediators, mechanisms
and pathways

DM and the musculoskeletal system
Conditions more frequently in DM
Diabetic cheiroarthrophaty (stiff hand
synd)
Trigger finger (flexor tenosynovitis)
Dupuytren’s contracture
Carpal tunnel syndrome
Adhesive shoulder capsulitis (frozen
shoulder)Calcific shoulder tendonitis
Reflex sympathetic dystrophy (
shoulder-hand syndrome)
Diabetic osteoarthrophaty or
Charcot's or neuropathic arthropathy
Conditions Sharing Risk Factors of DM
Diffuse Idiopathic Skeletal
Hyperostosis (DISH)
Gout/ Pseudo gout
Osteoarthritis
The impact of Metabolic Syndrome
on the musculoskeletal system
Obesity and the musculoskeletal
system
Musculoskeletal conditions associated
with obesity
OA (knee, hip, hand)
Low Back Pain
Diffuse idiopathic skeletal hyperostosis
(DISH)
Gait disturbance
Soft tissue conditions (for example,
carpal tunnel syndrome, plantar
fasciitis)
Osteoporosis ?
Gout
Fibromyalgia
Connective tissue disorders
(rheumatoid arthritis) .

Musculoskeletal disorder With diabetes Without diabetes
*Incidence estimate over 5 years.
Adhesive capsulitis
(frozen shoulder)5–8 11–30% 2–10%
Limited joint mobility9–11 8–50% 0–26%
Dupuytren’s
contracture12–15 20–63% 13%
Carpal tunnel
syndrome16,17 11–16% 125/100000*
Flexor tenosynovitis18 11% <1%
Diffuse idiopathic skeletal
hyperostosis DISH 10,15 13–49% 1.6–13%
Prevalence of musculoskeletal disorders
in patients with or without diabetes
(Reverse the equation for reciprocal diagnosis?) ‫والزكاة‬ ‫القطر‬ ‫مثال‬

Musculoskeletal manifestations
of diabetes mellitus
Pathogenesis
Effects of hyperglycemia:
1- Chronic inflammation
2- Metabolic changes (> DM 1)
3- Glycation of Collagen

Blood sugar and inflammation
the vicious cycle
Anatomy of the Vicious Cycle
Dr. Richard K. Bernstein,
the following equation is the vicious cycle of blood sugar
and inflammation:
Inheritance + inflammation + fat in the blood feeding the
liver = insulin resistance = elevated serum insulin levels =
fat cells to build even more abdominal fat = rise in
triglycerides in the liver’s blood supply = enhanced
inflammation = increased insulin levels due to increased
resistance to insulin
Researcher Mario Kratz, PhD,
a chronic low-grade inflammation plays a role in ALL major diseases:
Heart disease, diabetes, autoimmune disorders, arthritis, fibromyalgia, generalized
inflammation, and certain cancers.
Additionally, he confirms from his findings that inflammation causes insulin resistance
the main cause of type 2 diabetes.
SALIX ALBA

Obesity
Free fatty acids (NEFA)
Triglycerides
Hyperinsulinemia
Systemic Insulin
resistance
Systemic Insulin
resistance
Kidney
Musculoskeletal
Vessels
DM 2
Metabolic disorders
Metabolic syndrome
Triggering adipose
tissue inflammation
Local insulin
resistance
Adipose tissue
Macrophages Liver
Local insulin
resistance
Lipogenesis
Diabetes & Inflammation—the Vicious Cycle
Anatomy of the Vicious Cycle Dr. Richard K. Bernstein
Chronic low-grade inflammation plays a role in all major diseases including musculoskeletal manifestations
Phagocytosis + Pro inflammatory
mediators
Adipokines
1- Leptin (pro-inflammatory)
2- Adiponectin (anti-inflammatory).
Hyperglycemia
Blood sugar and inflammation - the vicious cycle

Galectin-3 blood levels are elevated in human and rodent obesity
Galectin-3 directly impairs insulin action in myocytes, adipocytes, and hepatocytes
Galectin-3 treatment causes systemic insulin resistance in vivo
Galectin-3 loss of function improves insulin sensitivity in obesity

Sedentary Lifestyle
Caloric overload, High Carb-Sugar, Inactivity, Stress, Sleep, Obesity, Drugs, etc
5- 83% Type 2 diabetes
Insulin, Not Cholesterol, Is the True Culprit in Heart Disease
February 18, 2017 | 6,928 views - Dr. Joseph Mercola
Reaven GM. Physiol Rev. 1995;75:473-486
Clauser, et al. Horm Res. 1992;38:5-12.
10- polycystic Ovary
Syndrome
(PCOS)
Insulin Resistance syndrome
Hyper insulinemia - Insulin toxicity
1- Direct damage blood vessels
Intima –neoangiogenesis –plaque -
3- High blood pressure
Mg loss in urine –> spasm of blood
vessels – salt water retention
Sympathetic nervous system
4- Heart disease & failure
Endothelial dysfunction, coagulopathy,
Hypertension , coronary heart disease.
6- Obesity (abdominal),
Lipogenesis - Dyslipidemia
9- Osteoporosis
8- Certain types of cancer
as colon, breast & prostate
INSULIN
RESISTANCE
(Toxicity)
12- Ch. Inflammation
Glucose - NEFA -Triglycerides
7- Insulin-Leptin-Ghrelin
(Hunger pain)2- Coagulation & fibrinolysis
disorders
11- Higher risk of Alz.D,
Nephropathy, etc

Signs and symptoms of
chronically elevated insulin:
1- Fatty liver
2- Unexplained Weight Gain
abdominal obesity
3- Hunger and cravings
4- Elevated blood sugar
5- Acne and pores on the face
testosterone
6- Menstrual Irregularities
7- Polycystic ovarian syndrome
8- Hirsutism , scalp hair loss in
women
as in male pattern
9- Acanthosis nigricans
10- Skin tags
11- Increased risk of gout.
fructose convert too uric acid
12- High blood pressure
13- Puffy swollen ankles
sodium and water
Vascular & heart disease
Fatty liver
Polycystic ovarian disease (PCOS)
Acanthosis nigricans -
Acne - large pores - faceSkin tags
Do You Know Your Insulin Level ?
October 23, 2013 by David Spero, BSN, RN
Hirsutism
Abdominal obesity
Elevated blood sugar

Origin of Inflammation:
There are many unknowns in medicine but what causes Inflammation we do know is:
Sugar, Omega 6, Lack of exercise
1- Environmental chemicals
2- Excessive chronic stress
3- Infections, allergies (food and environmental)
4- High glucose levels
5- Excessive abdominal fat
6- High carbohydrate and sugar foods
7- High Omega 6
8- Unhealthy unnatural processed food.
9- Too little or too much physical activity (everything in life needs to be in balance in
order to achieve and maintain wellness)
The question still perplexing scientists is, which came first, the fat or the
inflammation?
Musculoskeletal manifestations of diabetes mellitus
(Pathogenesis 1– Chronic inflammation)

1- Glycosylation (Glycation) of proteins
2- Micro vascular abnormality
(Blindness, Renal failure, and Neuropathy),
3- Macro vascular abnormality
(risk for myocardial infarction, stroke, and lower limb amputation )
4- Accumulation of extracellular matrix (ECM) and soft tissue
More seen in longstanding type I
Some complications have direct association
(Pathogenesis 2 – Metabolic changes)

GLUCOSE and other reducing sugars
React with proteins by a non-
enzymatic, post-translational
modification process called (non-
enzymatic glycosylation or
Glycation).
Non-enzymatic glycosylation or Glycation
Advanced-Glycation end-products (AGEs) :
The sugar-derived carbonyl group adds to a free amine, forming a reversible
adduct which over time rearranges to produce a class of products termed
advanced-Glycation end-products (AGEs)

Hyperglycemia
Advanced Glycosylation
End product (AGEs)
Micro & Macro vascular
damage
Collagen Dysfunction
(Glycated protein - Collagen - LDL –
LDH - Etc…)
AGEs inhibitor
Amino guanidine
(Pathogenesis 3 – Collagen Glycation)
->> dysfunction + micro-macro vascular insult
Glycation

1- AGEs causes micro and macro vascular complications
-Increased vascular permeability.
- Increased arterial stiffness
- Inhibition of vascular dilation by interfering with nitric oxide.
2- Oxidizing LDL.
3- Binding cells — including macrophage, endothelial, and mesangial — to induce
the secretion of a variety of cytokines.
4- Enhanced oxidative stress. — cell dysfunction
Advanced Glycosylation End product (AGEs)
pathological effects
AGEs result from early Glycolysation - Accumulate in tissue - Damage extra and intra
cellular proteins -There are receptors on cell surface for AGEs belong to IG receptors
- Signaling lead to cell dysfunction

Glycolysation of collagen
fiber
Increase collagen crosslink
Increase in hydration
Increased formation
Advanced Glycosylation
End product (AGEs)
(Pathogenesis 3 – Collagen Glycation)
->> dysfunction + micro-macro vascular insult

Classification:
1- Condition limited to DM
Diabetic Muscle Infarction
2- Conditions Sharing Risk
Factors of DM
Diffuse Idiopathic Skeletal
Hyperostosis (DISH)
Gout/ Pseudo gout
Osteoarthritis
3- Conditions more frequently in
DM
Diabetic cheiroarthrophaty (stiff
hand synd)
Trigger finger (flexor
tenosynovitis)
Dupuytren’s contracture
Carpal tunnel syndrome
Adhesive shoulder capsulitis
(frozen shoulder)
Calcific shoulder tendonitis
Reflex sympathetic dystrophy (
shoulder-hand syndrome)
Diabetic osteoarthrophaty or
Charcot's or neuropathic
arthropathy
The Musculoskeletal manifestations of
Diabetes Mellitus

The most disabling of the common musculoskeletal problems.
Progressive, painful restriction of shoulder movement, especially
external rotation and abduction.
The thickened joint capsule is closely applied and adherent to the
humeral head, resulting in considerable reduction in the volume of
the glenohumeral joint (fig 1).
The natural history of the disease is characterized by three distinct
phases: painful, adhesive, and resolution phases.
5 Adhesive capsulitis appears at a younger age in patients with diabetes
and is usually less painful,6 although it responds less well to treatment
and lasts longer.7
Adhesive capsulitis is associated with the duration of diabetes and
age.10,11
Figure 1 : Shoulder arthrogram showing a contracted and adherent joint capsule in adhesive capsulitis.
Diabetic patients with frozen shoulder are more likely to have other diabetic complications such as limited joint mobility than
diabetics without a frozen shoulder, although this may be explained by age.10,11
Most cases of adhesive capsulitis will resolve over time, but, in the interim, management consists of adequate analgesia and
intra-articular corticosteroid injections in the painful early stages if required. Corticosteroid injections may increase blood sugar
levels in diabetics over the 24–48 hour period after the injection, and therefore blood sugar monitoring and contingency plans for
elevated blood sugar levels should be considered. Distension or manipulation under anaesthesia are occasionally considered.
An appropriately graded, regular physiotherapy programme should be maintained, after the painful phase, throughout the course
of the condition.
Adhesive capsulitis
Also known as frozen shoulder, shoulder periarthritis, or obliterative bursitis

Frozen shoulder or adhesive capsulitis
Most common shoulder involvement
10-29% diabetic patients, bilateral, elderly
Stiffness Glenohumeral joint
Reversible contraction joint capsule
See in hyperthyroidism, Addison and Parkinson
Clinical manifestations of Adhesive capsulitis
Progressive and painful manner
Pain at night initially
Three phase:(a) Pain (b) Stiffness (c) Recovery
Diagnostic criteria by Pal: Shoulder pain at least one month, impossibility
lying's one shoulder, limited active and passive movement
Decreased range of motion in abduction and external rotation then internal
rotation
Adhesive capsulitis

Treatment:
1- Analgesic
2- Physiotherapy
3- Local CS injection
4- Arthroscopy release
Adhesive capsulitis

D Khalid Shoora
DM. uncontrolled

Three times more frequent in DM (type II)
Coexist with adhesive capsulitis
Deposit Ca hydroxy apatite
Ca deposition in rotator cuff tendons
60% asymptomatic
Calcific shoulder tendonitis

Intense burning pain, stiffness, swelling,
and discoloration that most often affects
the hand
Pain from shoulder to hand
Swelling of affected limb
Skin change: hair growth, shiny skin,
color, temperature
Increased sensitivity to pain and touch
Vasomotor instability
Transit patchy osteoporosis
Complex regional pain syndrome (CRPS)
Previously Known as reflex sympathetic dystrophy (RSD), Sudeck's atrophy,
shoulder-hand syndrome, or causalgia.

The exact cause of CRPS is unknown.
One theory is that a "short circuit" in the
nervous system is responsible. This "short
circuit" causes over activity of the
sympathetic nervous system which affects
blood flow and sweat glands in the affected
area.
Symptoms most commonly occur after
injury or surgery. Other causes include
pressure on a nerve, infection, cancer, neck
problems, stroke, or heart attack.
Complex Regional Pain Syndrome CRPS
(Reflex Sympathetic Dystrophy RSD)

Stage I: Acute
Stage I may last up to 3 months. Burning pain and increased sensitivity
to touch are the most common early symptom of CRPS. This pain is
different —more constant and longer lasting —than would be
expected with a given injury. Swelling and joint stiffness usually follow,
along with increased warmth and redness in the affected limb. There
may be faster-than-normal nail and hair growth and excessive
sweating .
Acute stage CRPS, 2 months after injury
Stage II: Dystrophic
Stage II can last 3 to 12 months. Swelling is more constant and skin
wrinkles disappear. Skin temperature becomes cooler. Fingernails
become brittle. Pain is more widespread, stiffness increases, and the
affected area becomes more sensitive to touch.
Stage III: Atrophic
Stage III occurs after 1 year. The skin of the affected area becomes pale,
dry, tightly stretched, and shiny. The area is stiff and there is less hope of
getting motion back. Pain may decrease and the condition may spread to
other areas of the body
Complex Regional Pain Syndrome CRPS
(Reflex Sympathetic Dystrophy RSD)
There are two types of CRPS:
Type 1 occurs after an illness or injury
that did not directly damage a nerve
in the affected area
Type 2 follows a distinct nerve injury
Although the triggers vary, both types
of CRPS have the same symptoms
and go through the same three
stages of disease.

8% to 50% all type I DM, 45%-70% type II
Associated and predictor of other
complication
Thick, tight, waxy skin, begin in MCP&PIP 5
Like systemic sclerosis
Limited joint mobility( finger flex and extend)
The association between the hand
abnormality and the duration of diabetes but
not age or sex is a consistent finding
Biopsy specimens of involved skin show
pronounced thickening of periarticular rather
than articular collagen, which may be due to
non-enzymatic glycosylation of collagen.13
cause Prayer sign is
Flexion contracture of fingers
nability of the two palms to
come completely together
Treatment:
1- Glycemic control
2- Physical therapy
3- NSAIDs with caution
Diabetic cheiroathrophathy
or diabetic stiff hand or limited mobility joint
syndrome

Flexor tenosynovitis (trigger finger or stenosing
tenovaginitis) is caused by:
fibrous tissue proliferation in the tendon sheath
leading to limitation of the normal movement of the
tendon.
The prevalence of flexor tenosynovitis is estimated
at 11% in diabetic patients, compared with <1% in
non-diabetics.29
There is also an increased incidence in people with
impaired glucose tolerance.30 Flexor tenosynovitis is
associated with the duration of diabetes but not
age.29
A corticosteroid injection into the symptomatic
flexor tendon sheath is often curative
Non infected flexor tenosynovitis

Incidence:
2.5 to 9.4% of all hand infections
Risk factors:
diabetes, IV drug use, immunocompromised patients
Staph aureus (40-75%) most common, MRSA (29%)
pain and swelling - warmth and erythema of the involved digit
- Kanavel signs (4 total) - flexed posturing of the involved digit
- tenderness to palpation over the tendon sheath - marked pain
with passive extension of the digit - fusiform swelling of the
digit
Treatment:
Nonoperative (rare)
Operative I&D followed by culture-specific IV antibiotics once
suspected (orthopaedic emergency)
no improvement after 24 hours of non-operative treatment
(confirmed diagnosis)
Complications:
Stiffness - Tendon or pulley rupture - Spread of infection - Loss
of soft tissue - Osteomyelitis
Infected flexor tenosynovitis

Catching sensation or locking phenomena
Pain in affected finger
Thumb, then third and forth
5%-36% type I, II (2% normal)
Palpable nodule overlying MCP joint
Thickening along the affected flexor tendon
Prevalence related to duration of DM
TF in 3 or more finger highly suggestive for DM
Treatments:
1-Change of activity
2- Splint
3- Use of NSAIDs with caution
4- Local CS injection
5- In severe case surgery
Trigger finger

Treatment
Aimed at reducing inflammation, preserving
movement in the thumb and preventing recurrence by
treatment early.
De Quervain's tenosynovitis starts during pregnancy
and lactation.
Medications
To reduce pain and swelling, pain relievers,
injections of corticosteroid
Therapy
Immobilizing
Avoiding repetitive thumb movements
Avoiding pinching with your thumb
Applying ice to the affected area
Surgery
Stenosing tenovaginitis
De Quervain's tenosynovitis

Thickening, shortening, fibrosis of palmar facia
Nodule along the facia
causes flexion contractures of the finger
Usually fourth but may be seen II to V fingers
16% to 42% of all DM more in elderly
May be seen in early stage
Prevalence more in longstanding DM
More in third and fourth finger
More in women
Manifestations are more severe in men
Treatments:
1- Intralesional injection of CS
2- Surgery
3- Physical therapy
4- Some studies show benefit from injection of
collagenase Clostridium Histolyticum
Dupuytren’s contracture

20% of diabetic patients more in women
More in obese
Median nerve entrapment
Caused by diabetic-induced connective tissue
alteration
Tinel’s sign, Phalen’s test
In dubious case Electrophysiological studies
helpful
Treatments:
1- Splint, NSAIDs
2- Injection CS: response may be temporary and
poorer in DM
3- Release surgery: post operative recovery is
worse
Carpal Tunnel syndrome

Characterized by localised or diffuse pain, usually with
associated swelling, trophic changes, and vasomotor
disturbances,31 with impaired mobility of the affected region.
There have been difficulties with the definitions of reflex
sympathetic dystrophy, and the cause, pathogenesis, and natural
history are unclear.
The condition may occur spontaneously, or after minimal
trauma—following surgery or a fracture.
Concurrent medical conditions may predispose to reflex
sympathetic dystrophy, including diabetes mellitus,
hyperthyroidism, hyperparathyroidism, and type IV
hyperlipidaemia.32
A variety of treatments have been used with anecdotal success,
including analgesics, physiotherapy, intravenous
bisphosphonates, calcitonin, oral corticosteroids, and
sympathetic ganglion blocks.32
The outcome is usually good, although some patients develop
chronic pain and contractures.
Reflex sympathetic dystrophy
also known as algodystrophy, Sudeck’s atrophy, and Complex regional pain
syndrome (CRPS)

Metaplastic calcification of spinal
ligament
Osteophyte formation
Disc space, sacroiliac and facet
joint: normal
Thoracic spine most commonly
affected
May be accompanied by generalized
calcification of other ligament
Diffuse idiopathic skeletal hyperostosis (DISH)
also known as ankylosing hyperostosis or Forestier’s disease

Unknown etiology
A proposed mechanism of causation is the
prolonged and high levels of insulin or insulin-
like growth factors occurring in diabetic
patients, stimulating new bone growth, and
may explain the higher prevalence in type 1
compared with type 2 diabetes (ratio 3:1).
IN DM patients more than normal
Association with type II DM
More in obese patients
Pain is not prominent symptoms
Complaint stiffness in neck and back
Decreased range of motion
Diffuse idiopathic skeletal hyperostosis (DISH)
also known as ankylosing hyperostosis or Forestier’s disease

Diabetic osteoarthropathy
Rare: 0.1% to 0.4%
Both type DM
Patients over the age of 50 who have had diabetes
for many years and have existing neuropathic
complications, average duration 15 years
Advanced peripheral neuropathy
A reduction in the normal afferent protective neural impulses, and
therefore loss of protection from trauma to the joint leads to
progressive, painless joint destruction
Weight-bearing joints such as the foot, ankles, and
knees; joints such as the hand and wrist are rarely
affected.35
Loss of sensation in involved joint
Inadvertent micro trauma to joint
Consecutive degenerative change
Severe destruction, lytic joint changes
Most affect pedal bones
Feet: Charcot’s arthropathy
Neuropathic (Charcot’s) joints

Clinically
Warmth and erythema mimic osteomyelitis or septic arthritis, but the absence of fever,
elevated white cell count, and elevated erythrocyte sedimentation rate helps to differentiate the
latter two conditions.
Erythema, swelling, hyperpimentation
Purpura, soft tissue ulcer
Joint loosening, instability, joint deformity
Often no history of trauma
Diagnosis
Based on radiographic findings
Symptoms often milder than view of X-ray
X-ray subluxation, bone fragment, osteolysis
Periosteal reaction, deformity, ankylosis
CT scan is insensitive
MRI and bone scintigraphy adjuncts X-ray
DD: Inflammatory, degenerative, infections, tumors, DVT
Treatments:
1- Optimizing glycaemic control and regular foot care and review, particularly in those
with grossly impaired sensation.
2- The use of orthotics and crutches can relieve pressure on the affected joints during
ambulation.35
3- Occasionally surgery may be required if complicated fractures develop.
4- Osteoporosis - Bisphosphonate -Calcitonin may be useful
Feet: Charcot’s arthropathy

Figure 8
Bilateral calcified Achilles tendons in a patient with diabetes.
Rates of hyperostosis increase with age in both the normal and diabetic
populations, although the age related increase in incidence begins earlier in
diabetics.6 Management consists of education, diabetic control, and
physiotherapy.

Figure 11
Bilateral painless ulcers in a patient with diabetic
peripheral neuropathy.
Figure 12
The nail through the sole of this slipper (see arrow) worn by a
patient with diabetic peripheral neuropathy, was only noticed
at the end of the day when the slipper was romoved.

Alia moh
Female 53 y old
DM type 2

Rare condition
Spontaneous infraction with no history of
trauma
Patients with long history of poorly
controlled DM
More in insulin requiring patients
Most patients show microvascular
complications like neuropathy, retinopathy,
nephropathy
Acute onset of pain and swelling on
affected M
Over days to weeks
Usually thigh or calf
Varying degree of tenderness
CPK may be normal or increased
Diabetic muscle infarction
D&D:
Tumor, muscle infection/abscess,
localized myositis, osteomyelitis,
thrombosis
CT Scan in insensitive
MRI show high signals in muscle in
T2
When incisional muscle biopsy?
Only to rule out infection and
malignancy(culture for atypical
organisms)
Treatments: rest, analgesic

Adisabling illness that is distinct from other forms of diabetic
neuropathy.
Muscle weakness and wasting,
Diffuse, proximal lower limb muscle pain,
Asymmetrical loss of tendon jerks.
The shoulder girdle may be affected, but less commonly (fig
13).
Typically occurs in older men with type 2 diabetes
Often associated with weight loss sometimes as much as 40%
of premorbid body mass.
The exact cause and incidence of diabetic amyotrophy is
uncertain.
It is a diagnosis of exclusion: sinister causes must be sought
and excluded because of the clinical picture of weight loss and
new neurological signs.
Management:
Stabilizing glycaemic control and use of physiotherapy.
Most cases improve, but the improvement is gradual and often
incomplete.36
Figure 13
Diabetic amyotrophy of the shoulder girdle.
Diabetic amyotrophy

Other diseases with DM
Osteoporosis
Osteoarthrosis
Hyperurecemia

The complications of diabetes mellitus are
numerous & multisystemic including the
musculoskeletal system.
The long term metabolic consequences of
diabetes mellitus stay behind Several
rheumatic conditions
Higher levels of diabetic complications is
due to poor glycemic control
Pharmacotherapy, diet, regular exercises
and sensible physiotherapy programmes
should be the cornerstone of diabetes
management
Conclusions

The incidence and prevalence of diabetes mellitus is rising.
About 50% of people with diabetes mellitus are unaware of their condition.
Approximately 25% of all patients with diabetes undergoing surgery are undiagnosed on
admission to hospital.
Patients with diabetes have a higher risk of cardiovascular insult and a higher
perioperative risk.
Surgeons and anaesthetists should be familiar with the risks of the diabetes, surgery and
anesthesia.
In emergency situations or non-elective cases insulin, glucose and potassium infusions
(blood glucose control + rehydration) before surgery
Prone to post operative complications, infection, wound care and bone healing
Conclusions
Patients with Diabetes Undergoing Surgery

Beyond the mortality and the respiratory and thromboembolic events
Infection is the main problem in Obesity & DM
A study with 7181 TKA and THA patients
1- increase infection rate from 0.57% in normal to 4.66% in morbid obesity
2- Diabetes doubled the infection rate, independent of the presence of obesity
3- In patients with morbid obesity and diabetes the infection rate was 10%
The authors questioned whether it was justified to operate on these patients
But it seems of the utmost importance not to operate on these patients unless the
diabetes in completely under control
The patient information step must include this infection risk, which is relatively higher
than in patients with a normal BMI. Since this risk is correlated to diabetes . Diabetes
must be well controlled and managed during the entire perioperative period
Conclusions
Patients with Diabetes Undergoing Surgery
Infection risk

How to control
Diabetes Mellitus

How to control Diabetes Mellitus
Lifestyle diseases can be reversed and cured
Therapeutic lifestyle change Rather than
treating risk factors by drugs for life
Prevent rather than treating Risk factors

How to control Diabetes Mellitus
Therapeutic lifestyle change
Stimulate insulin production :
1- Sunlight ->> circadian rhythm (Melatonin- Insulin)
2- Vitamin D ->> immunosuppressive (B cells)
(type 1 diabetes + 17% type 2 diabetes)
3- Drugs ->> Insulin
Improve insulin sensitivity :
1- Calcium ->> VGCC (Voltage gated calcium channel)
2- Exercise ->> Depletion of stores
3- Diet ->> LCHF vs. IF (Intermittent fasting)
(83% type 2 diabetes)
4- Drugs ->> Glucobay – Glucophage
Sunlight +Vitamin D + Calcium + Exercise + Diet
= Drugs for diabetes - its side effects

Rule of diet - LCHF vs. Intermittent fasting

The link between chronic hyperglycemia and vascular damage
has been established by four independent biochemical
abnormalities:
1- Increased polyol pathway flux,
2- Increased formation of advanced glycation end-
products (AGEs),
3- Activation of protein kinase C(PKC),
4- Increased hexosamine pathway flux.
These seemingly unrelated pathways have an
underlying common denominator: Overproduction
of superoxide by the mitochondrial electron transport
chain.
Mitochondrial reactive oxygen species (ROS) partially inhibit
the glycolytic enzymes glyceraldehyde-3-phosphate
dehydrogenase, which diverts increased substrate flux from
glycolysis to pathways of glucose over utilization. Preliminary
experimental evidence in vivo suggests that this new
paradigm provides a novel basis for research and drug
development.
Pathophysiological mechanisms of diabetic angiopathy
Author links open overlay pane lHans-PeterHammes
https://doi.org/10.1016/S1056-8727(02)00275-1Get rights and content
The sequelae of chronic hyperglycemia in diabetes of all phenotypes are divided into microvascular and
macrovascular complications.
Microvascular disease causes blindness, renal failure, and neuropathy, and diabetes-accelerated
Macrovascular disease causes excessive risk for myocardial infarction, stroke, and lower limb
amputation.

How to reduce diabetic
angiopathy
Figure 3. Oxidative defense strategies. CAT:
catalase; GPx: glutathione peroxidase; SOD:
superoxide dismutases.

How to reduce diabetic angiopathy

Musculoskeletal manifestations of diabetes mellitus

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