Diabetes Pearls Issue4

8/22/2019 Diabetes Pearls Issue4

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Issue No. 4 July 20

Article 1 |Article 2 |Article 3 |Article 4 |Article 5 |Article 6 |Article 7 |Article 8 |Article 9 |Article 10

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Diabetic neuropathies Update on denitions, diagnostic criteriestimation of severity, and treatmentsSource: Tesaye S, Boulton AJM, Dyck PJ, et al. Diabetic neuropathies: update on denitions, diagnostic criteria, estimation o severity, and treatme

Diabetes Care 2010;33:22852293.

"Treatment o painul DPN almost exclusively consists o

symptomatic therapies, which improve the symptoms

without aecting underlying causes or natural history"

"An abnormality o nerve conduction tests, which is requently

subclinical, appears to be the frst objective quantitative indication

o diabetic sensorimotor polyneuropathy"

Diabetes Care 2010

Classifcation and defnition

Diabetic neuropathies are heterogenous through their symptoms, pattern o neurologic involvement, course, risk covariat

pathologic alterations, and underlying mechanisms.
http://ppts/ppt1.ppthttp://ppts/ppt1.ppt


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Diabetic sensorimotor polyneuropathy (DSPN)

Thought to be the most common variety; this typical DPN is a chronic, symmetrical, length-dependent sensorimo

polyneuropathy attributable to metabolic and microvessel alterations because o chronic hyperglycemia exposure a

cardiovascular risk covariates

Total hyperglycemic exposure is perhaps the most important risk covariate, and, hence, the variety has been shown

be stabilized, perhaps even improved, by rigorous glycemic control

Autonomic dysunction and neuropathic pain may develop eventually

Atypical DPNs

Atypical DPNs dier rom DSPN in several important eatures, or instance, onset, course, maniestations, associatio

and maybe putative mechanisms.

These intercurrent varieties, developing at any time during the course o a patients diabetes, may exhibit be acu

subacute, or chronic onset o symptoms; though the course is usually monophasic or fuctuating over time.

The typical eatures are pain and autonomic symptoms; whilst altered immunity has also been suggested.

Estimating severity

A reliable objective and quantitative measure (i.e., nerve conduction abnormality) is suggested as the minimal criteria

the diagnosis o DSPN

The sum scores o various measures o neurologic signs, symptoms, neurophysiologic test abnormalities, or scores

unction o activities o daily living may provide an indication o the severity o DSPN.

Defnitions o minimal criteria or typical DSPN

Possible DSPN Presence o symptoms or signs o DSPN may include the ollowing

Symptomsdecreased sensation, positive neuropathic sensory symptoms (such as asleep numbness, prickling

stabbing, burning or aching pain) mainly in the toes, eet, or legs; OR

Signssymmetric decrease o distal sensation or clearly decreased or absent ankle refexes.


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Probable DSPN Presence o a combination o symptoms and signs o neuropathy include any two or more o t

ollowing:

Neuropathic symptoms; Decreased distal sensation, or ; Clearly decreased or absent ankle refexes

Conrmed DSPN Presence o an abnormality o nerve conduction and a symptom(s) or a sign(s) o neuropathy con

DSPN. In case nerve conduction is normal, a validated measure o small ber neuropathy may be used

Painul DPN

Peripheral neuropathic pain in diabetes is dened as pain arising as a direct consequence o abnormalities in the periphe

somatosensory system in patients with diabetes

The diagnosis o painul DPN in practice is a clinical one, relying on the patients description o pain

Symptoms o painul DPN are distal, symmetrical, oten associated with nocturnal exacerbations, and commonly describ

as prickling, deep aching, sharp, like an electric shock, and burning with hyperalgesia and requently allodynia up

examination

Symptoms are usually associated with the clinical signs o peripheral neuropathy

The severity o pain can be reliably assessed by the visual analog scale (VAS), the oldest and best validated measure, or

numerical rating scale, such as, the 11-point Likert scale (0 = no pain, 10 = worst possible pain).

Pharmacological management o painul DPNPharmacological management o painul DPN almost exclusively consists o symptomatic therapies (i.e., those improv

symptoms o painul DPN without aecting underlying causes or natural history)

Evidence supports the use o tricyclic antidepressants (e.g., amitriptyline), the anticonvulsants gabapentin and pregaba

and the serotonin and norepinephrine reuptake inhibitor duloxetine

Combinations o rst-line therapies may be considered i pain persists, despite a change in rst-line monotherapy

I pain is still not controlled adequately, opiods such as tramadol and oxycodone may be considered in a combinati

treatment.


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Issue No. 4 July 20

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Prevalence and characteristics of painful diabetic neuropathy in a largcommunity-based diabetic populationSource: Abbott CA, Malik RA, Van ross ERE, et al. Prevalence and Characteristics o Painul Diabetic Neuropathy in a Large Community-Based Diab

Population in the U.K. Diabetes Care 2011;34:22202224.

"Greater neuropathic pain levels are observed in type 2 diabetes,

in women, and in people of South Asian origin"

"One-third of all patients with diabetes in the communityhave painful neuropathic symptomatology, irrespective

of whether they have clinical neuropathy"

Objective

To assess, in the general diabetic population

The prevalence o painul neuropathic symptoms

The relationship between symptoms and clinical severity o neuropathy

The role o diabetes type, sex, and ethnicity in painul neuropathy.

Diabetes Care 2011


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Research design and methods

An observational epidemiological study o a large cohort o diabetic patients (N = 15,692) receiving community-bas

health care

Assessment o painul diabetic neuropathy (PDN) was done using neuropathy symptom score (NSS) and neuropa

disability score (NDS).

Results

The prevalence o painul symptoms (NSS 5) and PDN (NSS 5 and NDS 3) was 34 and 21%, respectively

Painul symptoms were ound to occur in 26% o patients without neuropathy (NDS 2) and 60% o patients with sevneuropathy (NDS > 8)

Adjusted risk o painul neuropathic symptoms in type 2 diabetes was double that o type 1 diabetes [odds ratio (OR) = 2

P < 0.001), which remained unaected by severity o neuropathy, insulin use, oot deormities, smoking, or alcohol

Compared with men, women exhibited 50% increased adjusted risk o painul symptoms (OR = 1.5, P < 0.0001)

Interestingly; despite less neuropathy in South Asians (14%) than Europeans (22%) and Arican Caribbeans (21

(P < 0.0001), painul symptoms were greater in South Asians (38 vs. 34 vs. 32%, P < 0.0001)

In addition, compared with other ethnic groups, South Asians without neuropathy maintained a 50% increased risk

painul neuropathy symptoms (P < 0.0001).

Conclusions

Regardless o the neuropathic defcit, one-third o all community-based diabetic patients have painul neuropa

symptoms

The prevalence o PDN was ound to be higher in patients with type 2 diabetes, women, and people o South As

origin

The study, accordingly, highlights a signifcant morbidity attributable to painul neuropathy, identiying key groups

screening or PDN.


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Issue No. 4 July 20


The KORA F4 Study Older subjects with diabetes and prediabetesare frequently unaware of having distal sensorimotorpolyneuropathySource:Bongaerts BWC, Rathmann W, Heier M, et al. Older subjects with diabetes and prediabetes are requently unaware o having distal sensorimo

polyneuropathy. Diabetes Care 2013;36:11411146.

"Older subjects with diabetes, and prediabetes, are frequently unaware of their

distal sensorimotor polyneuropathy (DSPN) status"

"Adequate attention should be given to professional foot examinations

in diabetic foot prevention practice"

Objective

To assess the prevalence o unawareness o distal sensorimotor polyneuropathy (DSPN), a severe complication o typ

diabetes, in prediabetes and diabetes in a sample o the older population.

Diabetes Care 2013


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Methods

The investigators determined glucose tolerance status amongst 61- to 82-year-old participants o the population-bas

KORA F4 Study (n = 1100)

The presence o bilaterally impaired oot-vibration perception and/or bilaterally impaired oot-pressure sensation w

identied to dene clinical DSPN

Answering no to the question, Has a physician ever told you that you are suering rom nerve damage, neuropat

polyneuropathy, or diabetic oot?, let DSPN case subjects to be considered unaware o their condition.

Results

Clinical DSPN was ound to be prevalent in 154 (14%) participants, 140 (91%) o whom were unaware o their disorder

With a prevalence o 23.9%; participants with combined impaired asting glucose and impaired glucose tolerance had

highest prevalence o DSPN - o these, 10/11 (91%) were unaware o having clinical DSPN

Participants with known diabetes exhibited an equally high prevalence o DSPN (22.0%), with 30/39 (77%) DSPN ca

subjects being unaware o having the disorder

Among subjects with known diabetes who reported having had their eet examined by a physician, 18/25 (72%) clini

DSPN case subjects were unaware o having DSPN.

ConclusionsThe ndings o the study highlights a high prevalence o unawareness o having clinical DSPN among the prediabetic a

diabetic groups

Besides, an insufcient requency o proessional oot examinations suggests inadequate attention to diabetic oot prevent

practice.


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An analysis of the ACCORD randomised trial Effect of intensivetreatment of hyperglycemia on microvascular outcomes in type 2diabetesSource: Ismail-Beigi F, Craven T, Banerji MA, et al. Eect o intensive treatment o hyperglycaemia on microvascular outcomes in type 2 diabetes

analysis o the ACCORD randomised trial. Lancet2010; 376:41930.

"Signifcant reductions in the development o peripheral

neuropathy, i urther sustained, suggest that intensive glycemia

therapy could decrease the risk o ulcers and number o uture leg

amputation"

"Microvascular benef ts o intensive therapy should weighagainst the increased total and cardiovascular disease-

related mortality, increased weight gain, and high risk or

severe hypoglycaemia"

Objective

To investigate whether reduction o blood glucose concentration reduces the rate o microvascular complications in patie

with type 2 diabetes.

Methods

In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, a parallel group, randomised trial, patients w

diabetes, high HbA1c concentrations (>75%), and cardiovascular disease (CVD) (or 2 cardiovascular risk factors) w

randomly assigned to intensive [target hemoglobin A1c (HbA1c) of


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Issue No. 4 July 20


In the current analysis, the pre-specifed composite outcomes were: dialysis or renal transplantation, high serum creatin

(>2917 mol/L), or retinal photocoagulation or vitrectomy (rst composite outcome); or peripheral neuropathy plus t

frst composite outcome (second composite outcome)

In addition, 13 prespecifed secondary measures o kidney, eye, and peripheral nerve unction were also assessed

Both the investigators and participants were aware o treatment group assignment

The authors did analysis or all patients who were assessed or microvascular outcomes, based on treatment assignme

regardless o treatments received or therapeutic compliance.

Results

A total of 10251 patients were randomized to the intensive glycemia control group (n=5128) and to the standard gro

(n=5123). Intensive therapy was stopped earlier than study end due to higher mortality in that group, and patients we

transitioned to the standard therapy

At this transition, the rst composite outcome was recorded in 443/5107 (8.7%) patients in the intensive group vs. 444/5

(8.7%) in the standard group (p=100), and the second composite outcome was noted in 1591/5107 (31.2%) vs. 1659/51

(325%) (p=019)

Results were similar at the study end [rst composite outcome, 556/5119 (109%) vs. 586/5115 (115%) (p=042); and seco

1956/5119 (382%) vs. 2046/5115 (400%), respectively (p=012)]

Though intensive therapy did not reduce the risk o advanced measures o microvascular outcomes, it delayed the on

o albuminuria and some measures o neuropathy and eye complications

Six secondary measures at study end appeared to favour the intensive therapy (p


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Issue No. 4 July 20


Diabetic neuropathy Clinical manifestations and current treatmentSource: Callaghan BC, Cheng HT, Stables CL, et al. Diabetic neuropathy: clinical maniestations and current treatments. Lancet Neurol2012;11:5213

Diabetic neuropathy

Diabetes is by ar the most common cause o neuropathy

Distal symmetrical polyneuropathy (DSP) represents the most common maniestation o diabetic peripheral neuropa

(DPN), a prevalent, disabling disorder; though many patterns o nerve injury patterns like small-bre predominant neuropat

radiculoplexopathy, and autonomic neuropathy, can also occur

"Increasing evidence supports an association between

components o the metabolic syndrome, including prediabetes,

and neuropathy."

The only efective treatments or patients with distal

symmetrical polyneuropathy are glucose control

and pain management

The prevalence o diabetic neuropathic pain may be

higher than reported.

Lancet Neurol 2012


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Patients with DSP typically have one or more o the ollowing symptoms: numbness, tingling, pain, or weakness

Symptoms ollow the so-called stocking-and-glove distribution they begin in the eet and spread proximally in a leng

dependent ashion

Symptoms are symmetrical, and sensory symptoms are more prominent than motor involvement

The likelihood o which symptom predominates varies substantially rom patient to patient

Neuropathy is one o the main risk actors or alls in patients with diabetes; others being retinopathy and vestibu

dysunction

In addition, patients with severe DSP are at risk o ulcerations and lower-extremity amputations

Neuropathic pain is one o the most disabling symptoms in patients with DSP that is dicult to treat and thereore cau

substantial sufering and burden

Glucose control considerably decreases the development o neuropathy in patents with type 1 diabetes; however, the ef

is probably much smaller in those with type 2 diabetes

Whilst use o specic anticonvulsants and antidepressants is suggested or pain management in patients with DPN, a l

o other disease-modiying therapies, save or glucose control, or diabetic DSP makes identication o new modiable r

actors essential

Components o the metabolic syndrome, including prediabetes, are potential risk actors or neuropathy; however, stud

are needed to establish the causality related to neuropathy.


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Approach to the management of the patient with neuropathic painSource: Vinik A. The Approach to the Management o the Patient with Neuropathic Pain. J Clin Endocrinol Metab 2010;95:48024811.

The patient with neuropathic pain

Neuropathic pain occurs in about 1520% o people with diabetes; dened as pain arising as a direct consequence o

lesion or disease aecting the somatosensory systemDiabetic neuropathy pain is a difcult-to-manage clinical problem, oten associated with mood and sleep disturbance

A variety o other conditions can pretense as neuropathy including entrapments, asciitis, and claudication

While pain can derive rom damage to nerve bers, or rom mechanisms within the spinal cord, brainstem, and cereb

cortex, together involving a various excitatory and inhibitory neurotransmitters, the pathogenesis o damage to the p

mechanism is multiactorial and includes metabolic disturbances such as hyperglycemia, even impaired glucose toleran

dyslipidemia, oxidative stress, growth actor deciencies, microvascular insufciency, and autoimmune damage to ne

bers

The optimal approach to managing a patient with neuropathic pain is rst to understand and recognize the cause o p

and to use monotherapies or drug combinations directed at the dierent types o pain

Finally, therapy should be tailored and directed at the underlying pathogenesis o neuropathy i the outcome is to

successul.

"Pain resolution in an individual is complex, and need a holistic approach

to medicine, employing empathy, compassion, and understanding to

succeed in alleviating pain"

Pain syndromes in diabetes may be ocal or diuse, proximal or distal,

acute or chronic

Neuropathic pain must be distinguished rom nociceptive pain, which is

a consequence o trauma, injury, or infammation.

J Clin Endocrinol Metab 2010


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Effects of treatments for symptoms of painful diabetic neuropathySource: Wong M, Chung JWY, Wong TKS. Eects o treatments or symptoms o painul diabetic neuropathy: systematic review. BMJ2007;1-10.

"In the clinical setting, management of diabetic neuropathy

focuses on two aspects: disease modifying treatmentsuch as glycaemic control and the use of various kinds of

analgesics to reduce the intensity of the pain"

"Compared with newer generation anticonvulsants, oral tricyclic

antidepressants and traditional anticonvulsants are better for

short term pain relief"

Objective

To evaluate the eects o treatments or the symptoms o diabetic painul neuropathy.

BMJ 2007


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Method

A systematic review o double blind randomised trials

Primary outcome was dichotomous inormation or 50% or moderate reduction o pain

Secondary outcomes were 30% reduction o pain and withdrawals related to adverse events.

Results

Odds ratios (ORs) were calculated or achievement o 30%, 50%, or moderate pain relie and or withdrawals related

adverse eects

Twenty ve reports were included, which compared anticonvulsants (n=1270), antidepressants (94), opioids (329),

channel blockers (173), N-methyl-D-aspartate antagonist (14), duloxetine (805), capsaicin (277), and isosorbide dinitr

spray (22) with placebo

ORs in terms o 50% pain relie were 5.33 or traditional anticonvulsants, 3.25 or newer generation anticonvulsants, a

22.24 or tricylic antidepressants

ORs in terms o withdrawals related to adverse events were 1.51 or traditional anticonvulsants, 2.98 or newer generat

anticonvulsants, and 2.32 or tricylic antidepressants

ORs or ion channel blockers could not be calculated because o insufcient dichotomous data.

Conclusion

The most commonly used options to manage diabetic neuropathy include anticonvulsants and antidepressants

Evidence o the long term eects o oral antidepressants and anticonvulsants is still lacking.


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2013 Canadian diabetes association clinical practice guidelines NeuropathySource: Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2013 Clinical Practice Guideli

or the Prevention and Management o Diabetes in Canada. Can J Diabetes 2013;37(suppl 1):S1-S212.

The Canadian Diabetes Association 2013 Clinical Practice Guidelines or the Prevention and Management o Diabetes are intend

to guide practice, to enhance diabetes prevention eorts, and to reduce the burden o diabetes complications in people livi

with this disease.

This presentation highlights pertinent principles related to the complication o neuropathy.

Patients with diabetes should be oered timely diabetes education

tailored to enhance sel-care practices and behaviours

Optimal glycemic control is the key to the management o diabetes

Treatment in most patients with type 1 or type 2 diabetes should

be targeted to achieve an A1C

7.0% so as to reduce the risk o

microvascular complications and, i implemented early in the course

o disease, macrovascular complications o diabetes.

Screening or peripheral neuropathy should begin at diagnosis

o diabetes in patients with type 2 diabetes, and occur annually

thereater. However, in patients with type 1 diabetes, annual

screening should commence ater 5 years postpubertal duration o

diabetes.

Can J Diabetes 2013


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Individualize glycemic targets based on age, duration o diabetes, risk

o severe hypoglycemia, presence or absence o cardiovascular disease,

and lie expectancy

Antihyperglycemic pharmacotherapy is indicated i glycemic targets are

not achieved within 2 to 3 months o liestyle management

To screen or peripheral neuropathy, assess loss o sensitivity to the 10-gmonoflament or loss o sensitivity to vibration at the dorsum o the great

toe.

Diabetic neuropathy

The chronic hyperglycemia seen in patients with diabetes is associated with signicant long-term microvascular a

macrovascular complications

Detectable sensorimotor polyneuropathy develops in about 40% to 50% o people with type 1 or type 2 diabetes wit

10 years o the onset o diabetes

The timing o diagnosis may be important given that whilst clinical neuropathy is uncommon in people with type 1 diabe

within the rst 5 years ater the onset o diabetes, in contrast, people with type 2 diabetes may have neuropathy at the ti

o diagnosis

Risk actors or neuropathy include: elevated blood glucose levels, elevated triglycerides, high body mass index (BM

smoking and hypertension


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Foot ulceration, dependent on the degree o oot insensitivity, and amputation are two important and costly sequelae

diabetic neuropathy

Mononeuropathy, especially the carpal tunnel syndrome, is common in patients with diabetes and can be difcult

diagnose

Intensive glycemic control is eective both or the primary and secondary intervention o neuropathy in patients with ty

1 diabetes

Lower levels o blood glucose are associated with a reduced requency o neuropathy in patients with type 2 diabetes

It has been noted that simple physical examination screening tests, or instance the monolament and vibration percept

tests or neuropathy, perorm reasonably well or identication o neuropathy, and predicting its uture onset

The ollowing agents may be used alone or in combination or relie o painul peripheral neuropathy.

Anticonvulsants (pregabalin, gabapentin, valproate)

Antidepressants (amitriptyline, duloxetine, venlaaxine)

Opioid analgesics (tapentadol ER, oxycodone ER, tramadol)

Topical nitrate spray

Generally, ew patients have complete relie o painul symptoms with any treatment or neuropathic pain. A 30% to 5

reduction in baseline pain is considered to be clinically meaningul response.


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AAN Evidence-based guideline Treatment of painful diabetneuropathySource: Bril V, England J, Franklin GM, et al. Evidence-based guideline: Treatment o painul diabetic neuropathy. Neurology2011;76:17581765.

"The guidelines give a scientically sound and clinically relevant

evidence-based method or the treatment o painul diabetic

neuropathy"

Eective treatments or painul diabetic neuropathy are available, but

many have side eects that limit their useulness. Few studies have

sufcient inormation on treatment eects on unction and quality olie

Pregabalin is eective and should be oered or relie o painul diabetic

neuropathy

Venlaaxine, duloxetine, amitriptyline, valproate, gabapentin, opioids,

and capsaicin are probably eective and should be considered or

treatment o painul diabetic neuropathy.

Neurology 2011


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Objective

To develop evidence-based guidelines or the treatment o painul diabetic neuropathy.

Methods

A systematic literature review was perormed, with studies classied according to the American Academy o Neurolo

(AAN) classication o evidence scheme or a therapeutic article, and recommendations were linked to the strength o t

evidence

The research question: What is the ecacy o a given treatment to reduce pain and improve physical unction and qua

o lie in patients with painul diabetic neuropathy?

Results/recommendations

Anticonvulsants

I clinically apt, pregabalin should be oered or the treatment o painul diabetic neuropathy

Sodium valproate and gabapentin and should be considered or the treatment o painul diabetic neuropathy. Howev

sodium valproate is potentially teratogenic and should be avoided in diabetic women o childbearing age

There exists insucient evidence to support or reute the use o topiramate or the treatment o painul diabe

neuropathy

Oxcarbazepine, lacosamide, and lamotrigine should probably not be considered or the treatment o painul diabe

neuropathy.

Antidepressants

Amitriptyline, duloxetine, and venlaaxine should be considered or the treatment o painul diabetic neuropathy.

Venlaaxine may be added to gabapentin or a better response

There exists insucient evidence to support or reute the use o desipramine, fuoxetine, imipramine, or the combinat

o fuphenazine and nortriptyline in the treatment o painul diabetic neuropathy.


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Opioids

Dextromethorphan, tramadol, morphine sulate, and oxycodone controlled-release should be considered or the treatm

o painul diabetic neuropathy

Chronic use o opioids can lead to tolerance and requent dose escalation.

Other pharmacologic agents

Whilst capsaicin and isosorbide dinitrate spray should be considered or the treatment o painul diabetic neuropat

clonidine, mexiletine, and pentoxiylline should probably not be considered

Many patients are intolerant o the side eects o capsaicin, mainly burning pain on contact with warm/hot water or in weather

Lidoderm patch may be considered or the treatment o painul diabetic neuropathy

Insucient evidence exists to support or reute the useulness o vitamins and -lipoic acid in the treatment o pain

diabetic neuropathy.

Non-pharmacologic modalities

Percutaneous electrical nerve stimulation should be considered or the treatment o painul diabetic neuropathy

Electromagnetic eld treatment, low-intensity laser treatment, and Reiki therapy should probably not be considered

the treatment o painul diabetic neuropathy

There exists insucient evidence to support or reute the use o amitriptyline plus electrotherapy or treatment o pain

diabetic neuropathy.


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NICE clinical guidelines The pharmacological management oneuropathic pain in adults in non-specialist settingsSource: Neuropathic pain. The pharmacological management o neuropathic pain in adults in non-specialist settings. NICE clinical guideline 96; 201

Neuropathic pain is an unpleasant sensory and emotional

experience, and can have a signicant impact on a person's

quality o lie

Being resistant to many medications and/or because o

the adverse eects associated with eective medications;

neuropathic pain is oten difcult to treat

A number o drugs are used to manage neuropathic pain,

including antidepressants, anticonvulsants, opioids and topicaltreatments such as capsaicin and lidocaine, but the correct

choice o drugs, and the optimal sequence or their use, remains

largely indistinct.

Regular clinical reviews, which include assessment o pain reduction, adverse eects, daily activities and participation, mo

quality o sleep and overall improvement as reported by the person, should be perormed to assess and monitor the eectiven

o the chosen treatment.

"Treatment and care should consider patients' needs and preerences, whilst

giving them the opportunity to make inormed decisions"


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First-line treatment

Oral amitriptyline or pregabalin

Amitriptyline start at 10 mg/day, with gradual upward titration to an eective dose or the person's maximum tolera

dose o no higher than 75 mg/day (consider higher in consultation with a specialist pain service).

Pregabalin start at 150 mg/day (divided into 2 doses; a lower starting dose may be appropriate or some people), w

upward titration to an eective dose or the person's maximum tolerated dose o no higher than 600 mg/day (divided i

two doses)

Oral duloxetine as frst-line treatment or people with painul diabetic neuropathy; oer amitriptyline i duloxetine

contraindicated

Start duloxetine at 60 mg/day (a lower starting dose may be appropriate or some people), with upward titration to

eective dose or the person's maximum tolerated dose o no higher than 120 mg/day

Continue the treatment i there is satisactory improvement; consider gradually reducing the dose eventually i ther

sustained improvement

Consider oral imipramine or nortriptyline as an alternative, i amitriptyline, as frst-line treatment, results in satisactory p

reduction but the person is not able to tolerate the adverse eects.

Second-line treatment

Oer treatment with another alternative drug, rather than or in combination with the original drug, i satisactory p

reduction is not achieved with frst-line treatment at the maximum tolerated dose. Such decision should be based

inormed discussion with the patient

Consider switching to, or combine with, oral pregabalin, i the frst-line treatment was with amitriptyline (or nortriptyl

or imipramine)


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Consider switching to, or combine with, oral amitriptyline i frst-line treatment was with pregabalin (consider imipram

or nortriptyline as an alternative i the patent cannot tolerate the adverse eects o amitriptyline)

For people with painul diabetic neuropathy:

Consider switching to amitriptyline or pregabalin, or combine with pregabalin, i frst-line treatment was w

duloxetine

Consider switching to, or combine with, pregabalin, i frst-line treatment was with amitriptyline

Third-line treatment

Reer the patient to a specialist pain service and/or a condition-specifc service i satisactory pain reduction is not achiev

with second-line treatment

Whilst waiting or reerral:

Consider oral tramadol, instead o, or in combination with, the second-line treatment

For patients unable to take oral medication because o medical conditions and/or disability, consider topical lidoca

or localised pain

Tramadol monotherapy start at 50 to 100 mg not more oten than every 4 hours; i required, titrate upwards to an eect

dose or the person's maximum tolerated dose o no higher than 400 mg/day. More conservative titration may be requi

when tramadol is used as combination therapy.

Other treatments

It is recommended not to start treatment with opioids (such as oxycodone or morphine) other than tramadol without an assessm

by a specialist pain service or a condition-specifc service.


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Issue No. 4 July 20

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his continuing medical education program is intended only to enhance knowledge of the diseases and improve management skills of doctors. The usage of all knowledge/inforcquired/derived during or on account of this activity will be at their sole discretion/judgment, USV will not be accountable for any liability arising out of the use and for any other

ommission/omission.


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Diabetes Pearls Issue4