DIABETES MELLITUS: MUSCULOSKELETAL MANIFESTATIONS AND PREOPERATIVE CONSIDERATIONS FOR THE ORTHOPAEDIC SURGEON

by Dr. Giridhar boyapati

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.

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.

PATHOPHYSIOLOGY

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.

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.

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.

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.

PREVALENCE OF VARIOUS MUSCULOSKELETAL MANIFESTATIONS IN DIABETICS

DISORDERSINCIDENCE IN

DIABETICS

INCIDENCE IN

NON-DIABETICS

ADHESIVE

CAPSULITIS11- 30 % 2-10%

DUPUYTREN CONTRACTURE 16-42 % 13%

CARPAL TUNNEL

SYNDROME11-20% 0.05%

FLEXOR TENOSYNOVITIS 11% <1%

DISH 13-49% 1.6-13%

LIMITED JOINT MOBILITY 8-50% 0-26%

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.

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.

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.

WAGNER CLASSIFICATION OF DIABETIC FOOT ULCERS

.

GRADE 0 Intact skin but foot at risk patient education, foot wear

GRADE 1superficial ulceration, not

infected

External pressure relief: TCC,

Prefabricated pneumatic braces,

walking brace

GRADE 2deep ulceration with exposed

tendons, joints( superficial infection)

surgical debridement and

wound care

GRADE 3deep ulceration with exposed

bone with deep infection

surgical debridement,

antibiotics, wound care

GRADE 4 partial gangrenevascular evaluation,

amputation

GRADE 5 complete gangrene amputation

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.

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.

EICHENHOLTZ CLASSIFICATION OF CHARCOT NEUROARTHROPATHY

SATGECLINICAL RADIOLOGICAL

FEATURESTREATMENT

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

ADHESIVE CAPSULITISIncidence 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.

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.

• 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.

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.

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.

HAND MANIFESTATIONS OF

DIABETES MELLITUS

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.

• 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.

PRAYER SIGN

TABLE TOP SIGN

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

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.

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.

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.

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.

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.

• Analgesics

• Physiotherapy,

• Bis-phosphonates,

• calcitonin,

• oral corticosteroids, and

• sympathetic ganglion blocks.

• The outcome is usually good, although some patients develop chronic

pain and contractures.

DERMATOLOGICAL LESIONS

Bullosis diabeticorum

Granuloma annulare

Huntleys papules

Necrobiosis lipoidica diabeticorum

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.

PERI-OPERATIVE CONSIDERATIONS BY SYSTEM FOR DIABETICS

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

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

RENAL

Screening for Microalbuminuria and protenuria

Serum creatinine is not always a reliable indicator of renal

function

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.

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

INCREASED RISK OF WOUND COMPLICATIONS

PRE OPERATIVE HbAIC > 6.7%

POST OPERATIVE BLOOD GLUCOSE

CONCENTRATIONS > 200 mg/dl

RECOMMENDATIONS FROM

THE ENDOCRINE SOCIETY CLINICAL PRACTICE

GUIDELINES ON MANAGEMENT OFHYPERGLYCEMIA FOR

ORTHOPAEDIC PATIENTS

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.

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.

BLOOD GLUCOSE TARGETS IN NON CRITICAL CARE SETTING

A Pre-meal Target of < 140 mg/dl

Random BG < 180 mg/dl

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

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.

RECOGNITION AND MANAGEMENT OF HYPOGLYCEMIA IN HOSPITAL SETTING

If BG drops to below 70 mg/dl immediate therapy is required

to restore euglycemic state.