diabetes, musculoskeletal manifestations, orthopaedic

1. DIABETES MELLITUS:
MUSCULOSKELETAL MANIFESTATIONS
AND PREOPERATIVE
CONSIDERATIONS FOR THE
ORTHOPAEDIC SURGEON
by Dr. Giridhar boyapati

2. DIABETES MELLITUS
It is a disease of uncontrolled hyperglycemia.
Despite a more sophisticated understanding of the
pathophysiology of diabetes mellitus and despite of
pharmacological advancements that enable better glycemic
control, the prevalence of this disease and its devastating
sequele continue to rise.

3. Type 1 : autoimmune destruction of insulin producing beta
cells of the pancreas.
Patients are insulin deficient and prone to develop ketosis.
Type 2 : accounts for 90-95% of all cases.
Patients produce insulin but are unable to properly use it
due to end organ damage.

4. PATHOPHYSIOLOGY

5. NERVOUS SYSTEM
Motor, Sensory, Autonomic divisions of the nervous system
are adversely effected.
Diabetic Neuropathy most commonly manifests as
symmetrical peripheral polyneuropathy, with diminished
sensations in glove stocking distribution.
Isolated involvement of individual peripheral and cranial
nerves is less common.
Autonomic neuropathy causes gastrointestinal, gentourinary
and cardiovascular symptoms.

6. VASCULAR SYSTEM
microvascular and macrovascular disease.
Microvascular disease: development of neuropathy,
nephropathy, and retinopathy
Macrovascular disease: coronary artery disease,
cerebrovascular disease, stroke, peripheral arterial disease (
PAD) and lower extremity infection and amputation.
Uncontrolled hyperglycemia contributes to vasoconstriction, a
hyper coagulable state and arterial luminal stenosis.
PAD is more often bilateral and more rapidly progressive in
persons with diabetes than in those without disease.

7. IMMUNE SYSTEM
Altered polymorphonuclear leucocyte function.
DM causes :
1. Favorable environment for bacterial growth
2. Compromises fibrobalst function
3. Collagen synthesis
4. Interfere with wound healing and increase the
incidence of postoperative wound infections.

8. MUSCULOSKELETAL SYSTEM
High blood glucose causes increased collagen cross-linking
via Advanced Glycosilation End products which decrease
the solubility and digestibility of collagen.
This increases the stiffness of both collagen and the
structures built on a collagenous framework.

9. PREVALENCE OF VARIOUS
MUSCULOSKELETAL MANIFESTATIONS IN
DIABETICS
DISORDERS
INCIDENCE IN
DIABETICS
INCIDENCE IN
NON-DIABETICS
ADHESIVE
CAPSULITIS
11- 30 % 2-10%
DUPUYTREN CONTRACTURE 16-42 % 13%
CARPAL TUNNEL
SYNDROME 11-20% 0.05%
FLEXOR TENOSYNOVITIS 11% <1%
DISH 13-49% 1.6-13%
LIMITED JOINT MOBILITY 8-50% 0-26%

10. DIABETIC FOOT
Diabetic foot is susceptible to ulceration, infections,
neuroarthropathy and fractures.
15% lifetime risk of developing a foot ulcer.
5% risk of lower extremity amputation if diagnosed before
30yrs age( younger onset DM) and 7% in patients
diagnosed after 30 years ( older onset DM)
28-51% will require second amputation.

11. Evaluation through history and physical examination
A reduced or lost ankle jerk reflex is suggestive of neuropathy and
often is the earliest signs of diminished protective sensation.
Peripheral neuropathy can also identified by 128 hz tuning fork or 10 g
semmes weinstein monofilament.
Vascular examination must include examination of peripheral pulses
and Ankle Brachial Index ABI.
ABI ratio of systolic BP in ankle divided by systolic BP in the arm.
Normal ABI 0.91 to 1.3
A value of <0.91 indicative of obstruction
A value above >1.3 indicate poorly compressible vessels due to
calcification.

12. Ulceration is the most common cause of soft tissue
infections in patients with diabetes.
According to Boyko et al. the relative risk is increased by
sensory and autonomic neuropathy, greater BMI, poor
vision, refused skin oxygenation and foot perfusion, and
deformities of foot. Duration and type of diabetes, race,
smoking status, joint mobility have no correlation with risk of
foot ulceration.

13. WAGNER CLASSIFICATION OF
DIABETIC FOOT ULCERS
.
GRADE 0 Intact skin but foot at risk patient education, foot wear
GRADE 1
superficial ulceration, not
infected
External pressure relief: TCC,
Prefabricated pneumatic braces,
walking brace
GRADE 2 deep ulceration with exposed
tendons, joints( superficial infection)
surgical debridement and
wound care
GRADE 3
deep ulceration with exposed
bone with deep infection
surgical debridement,
antibiotics, wound care
GRADE 4 partial gangrene
vascular evaluation,
amputation
GRADE 5 complete gangrene amputation

14. TOTAL CONTACT CAST ( TCC) : used in Wagner grade 1
& 2. Require frequent follow up and weekly cast changes.
Complications include appearance of new pretibial,
malleolar, and foot ulcers.
PREFABRICATED PNEUMATIC WALKING BRACES. have
pressure adjusted air bladders lined with soft nylon material
that prevents abrasions and ulcerations.

15. CHARCOT NEUROARTHROPATHY
Progressive, non infectious disease seen in persons with sensory
neuropathy
Diabetes is the most common cause of charcot neuroarthopathy
Exact etiology is not known.
Theories :
Neurotraumatic theory proposes that loss of neuroprotection
leads to repetitive micro trauma.
Neurotrophic theory sympathetic neuropathy catalyses osteoclast
bone resorption and fragmentation.

16. EICHENHOLTZ CLASSIFICATION OF
CHARCOT NEUROARTHROPATHY
SATGE
CLINICAL RADIOLOGICAL
FEATURES
TREATMENT
STAGE 1
FRAGMENTATION
OR DISSOLUTION
swelling, warmth,erythema;
fractures,
dislocations;osteopenia
protected weight bearing,
follow-up
STAGE 2
COALESCENCE
reduced warmth and
swelling, resorption of
bone, early fusion and
sclerosis
protected weight bearing,
orthotic walker
STAGE 3
RECONSTRUCTION
consolidation of
deformity with joint
arthritis, subchondral
sclerosis
Plantigrade foot: custom inlay
shoes.
Non-plantigrade foot :
debridement,exostectomy,correcti
on or fusion with internal fixation

17. ADHESIVE CAPSULITIS
Incidence is 11-30% in diabetics when compared to 2-10% in non
diabetics.
Patients with Type 1 DM have higher rate of adhesive capsulitis
compared with type 2 DM.
Patients with diabetes also have :
1. worse response to nonsurgical treatment, including NSAIDS,
physical therapy and corticosteroids
2. Adhesive capsulitis appears at a younger age in patients with
diabetes
3. Usually less painful,6 although it responds less well to treat-ment
and lasts longer.

18. D.I.S.H / FORESTEIR’S
DISEASE
Commonly seen in Type 2 DM
Characterized by new bone formation,mostly involving
thoracolumbar vertebrae, as well as calcification of spinal
ligaments.
Degree of glycemic control does not correlate with incidence
or progression of the symptoms.
New bone appears to “flow” from one vertebra to the next,
and is more prominent on the right side of the thoracic
vertebra.

19. • Ossification of ligaments and tendons elsewhere may occur, such as the
skull, pelvis, heels, or elbows.
• 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.
• Associated pain in one third of patients who have hyperostosis of the
heels or elbows. Patients with hyperostosis of the spine may have
associated mild stiffness on arising in the morning, and 16% of affected
persons may develop dysphagia.
• In most cases affected persons have normal mobility of the spine and
may be asymptomatic, with the diagnosis of the condition an incidental
radiographic finding.

20. DIABETIC AMYOTROPHY
• It is characterized by muscle weakness and wasting, and by diffuse, proximal
lower limb muscle pain, and asymmetrical loss of tendon jerks. The shoulder
girdle may be affected, but less commonly.
• It typically occurs in older men with type 2 diabetes, and is often associated
with weight loss, sometimes as much as 40% of premorbid body mass.
• Management consists of stabilizing glycaemic control and use of
physiotherapy. Most cases improve, but the improvement is gradual and often
incomplete.

21. DIABETIC MUSCLE
INFARCTION
Common in type 1 DM
Acute onset of muscle pain and swelling. Most commonly
effecting thigh muscles and calf muscles.
A palpable mass has been reported in 34-44%
Serum creatine kinase levels elevated.
muscle biopsy: muscle fibre necrosis, edema, granulation
tissue.
medical treatment : anti platelet and anti inflammatory drugs.

22. HAND MANIFESTATIONS OF
DIABETES MELLITUS

23. Limited joint mobility/Diabetic Cheiroarthopathy
• It is characterized by thick, tight, waxy skin mainly on the dorsal aspect of the
hands, with flexion deformities of the
1. metacarpo-phalangeal and
2. interphalangeal joints
• Limited joint mobility can be shown clinically by the inability of the two palms
to come completely together, with the wrists maximally flexed, forming the
prayer sign .
• In the early stages, paraesthesias and slight pain develop.
• The symptoms increase very slowly, and greater pain, aggravated by movement
of the hands, may supervene.

24. • Biopsy specimens of involved skin pronounced thickening of periarticular
rather than articular collagen, which may be due to non-enzymatic glycosylation
of collagen.
• This condition is most commonly seen in type 1 diabetics, with a prevalence
of 8–50%,compared with 0–26% in controls
• Limited joint mobility is more prevalent in patients with diabetic
neuropathy
• Limited joint mobility and Dupuytren’s contracture are commonly found
in the same patient.

25. PRAYER SIGN

26. TABLE TOP SIGN

27. DUPUYTREN’S CONTRACTURE
• The palmar or digital thickening, tethering, or contracture of the hands
• In patients with diabetes, the ring and middle finger are more commonly affected,
compared with the fifth finger in patients without diabetes.
• The prevalence of Dupuytren’s contracture in diabetic patients ranges from 20 to
63%, compared with 13% in the general population.
• Among patients with Dupuytren’s contracture, 13–39% have diabetes.
• The contractures are generally milder in diabetics than in patients with
Dupuytren’s contracture who do not have diabetes

28. Treatment consists of
optimizing glycaemic control,
physiotherapy, and hand exercises if required, and
surgery only if function is severely affected.
The contractures are usually mild, however, and rarely require surgery.

30. CARPAL TUNNEL SYNDROME
Characterized by paraesthesia over the median nerve cutaneous distribution of the
thumb, index, middle, and lateral half of the ring fingers, which is often worse at
night.
The symptoms may be caused by:
compression of the median nerve within the carpal tunnel,
diabetic neuropathy,
or a combination of both
CTS is common in patients with diabetes, with an estimated prevalence of 11-16%,
compared with an incidence of about 125 per 100000 population over a five year
period.
About 5–8% of patients with CTS have diabetes.

31. CTS is more common in women than in men.
Treatment of CTS consists of the use of
simple analgesics,
splints
local steroid injections for the milder cases of compressive CTS.
Surgery is indicated in those patients who fail the above conservative measures.

32. TRIGGER FINGER
FLEXOR TENOSYNOVITIS
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.
Flexor tenosynovitis is associated with the duration of diabetes but not age.
A corticosteroid injection into the symptomatic flexor tendon sheath is often curative.

34. RELFEX SYMPATHETIC
DYSTROPHY
Characterized by localised or diffuse pain, usually with associated swelling, trophic
changes, and vasomotor disturbances, with impaired mobility of the affected region
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.

35. • Analgesics
• Physiotherapy,
• Bis-phosphonates,
• calcitonin,
• oral corticosteroids, and
• sympathetic ganglion blocks.
• The outcome is usually good, although some patients develop chronic
pain and contractures.

37. DERMATOLOGICAL LESIONS
Bullosis diabeticorum
Granuloma annulare
Huntleys papules
Necrobiosis lipoidica diabeticorum

38. PERI-OPERATIVE
CONSIDERATIONS
wound dehiscence
wound infection: superficial
and deep
fracture non-union
loss of fracture reduction
hardware and implant
failure
myocardial infarction
stroke
UTI
ILEUS
pulmonary embolism
hemorrhage
Increased transfusion
requirement.

39. PERI-OPERATIVE
CONSIDERATIONS BY
SYSTEM FOR DIABETICS

40. ENDOCRINE
Check HbA1C .
Evaluate daily glycemic control
Consider admission 1 day before surgery to optimize
metabolic control
Check blood glucose before anesthesia
If possible, the patient should be first on surgical schedule

41. CARDIO-VASCULAR
Recent MI. ( 6% rate of re-infarction or death if surgery is
performed within 3 months of a myocardial infarction)
Check ECG
Blood pressure : Pre Operative goal of < 140/90 mm Hg

42. RENAL
Screening for Microalbuminuria and protenuria
Serum creatinine is not always a reliable indicator of renal
function

43. NERVOUS SYSTEM ( A.N.S)
Autonomic neuropathy predisposes to Perioperative
hypotension
Diagnostic tests : Orthostatic blood pressure measurements
( fixed pulse indicate significant autonomic neuropathy)
Patients with autonomic neuropathy require careful
preoperative blood pressure and volume monitoring.

44. GASTRO-INTESTINAL
Diabetic gastroparesis:
1. increased risk of aspiration during intubation, even if the
patient has received nothing by mouth for 6 hrs before
surgery
2. postoperative ileus

45. INCREASED RISK OF WOUND COMPLICATIONS
PRE OPERATIVE HbAIC > 6.7%
POST OPERATIVE BLOOD GLUCOSE
CONCENTRATIONS > 200 mg/dl

46. RECOMMENDATIONS FROM
THE ENDOCRINE SOCIETY
CLINICAL PRACTICE
GUIDELINES ON MANAGEMENT OF
HYPERGLYCEMIA FOR
ORTHOPAEDIC PATIENTS

47. DIAGNOSIS AND RECOGNITION OF
HYPERGLYCEMIA AND DIABETES IN THE
HOSPITAL SETTING
All patients should have blood glucose testing
Patients without a history of diabetes with BG > 140 mg/dl
should be monitored with bedside testing for 24 to 48 hrs. If
BG is more than 140 mg/dl appropriate intervention
required.
All inpatients with known diabetes or hyperglycemia should
be accessed with HbA1C.

48. MONITORING BG IN THE
NONCRITICAL CARE SETTING
Timing of BG measurements should match the patients
nutritional intake and medication regimen.
Testing should be done before meals and at bedtime in
patients who are eating and every 4-6 hrs in patients who
are receiving nothing by mouth.

49. BLOOD GLUCOSE TARGETS IN
NON CRITICAL CARE SETTING
A Pre-meal Target of < 140 mg/dl
Random BG < 180 mg/dl

50. PHARMACOLOGICAL THERAPY
Insulin therapy preferred for glycemic control in diabetics
Oral hypoglycemic agents changed to insulin therapy for
majority of patients with type 2 DM at time of admission
In patients on insulin before admission, the dose should be
titrated.
Use of insulin sliding scale as a sole method of glycemic
control should be avoided.
Insulin therapy : combination of basal/intermediate acting +
rapid / short acting insulin

51. PRE OPERATIVE BG
CONTROL
All patients with type 1 DM who undergo any surgical
procedure should receive either continuos insulin infusion or
bolus dose.
Oral anti-diabetic drugs discontinued before surgery and
insulin therapy initiated.

52. RECOGNITION AND MANAGEMENT OF
HYPOGLYCEMIA IN HOSPITAL SETTING
If BG drops to below 70 mg/dl immediate therapy is required
to restore euglycemic state.