Diabetic complications Flashcards
What is diabetic amyotrophy?
it’s a well controlled DM or new onset diabetics who may not have other end organ damage but see ischemic injury from non systemic microvasculitis
What is the presentation of diabetic amyotrophy?
acute symmetric focal onset of pain followed by weakness in proximal leg and see autonomic failure and weight loss of >10%
Prognosis of diabetic amyotrophy?
condition progresses to involve contralateral limb and distal legs. Majority of pts will need ambulatory assistance device at some point progress is followed by partial to full recovery in most pts some may have lingering foot drop or neuropathic pain for years
Who gets diabetic amyotrophy?
>50 yrs DM2 or reasonably controlled A1c about 7.5%. They have acute or asymmetric focal proximal lower extremity pain associated with weakness
what must we keep on differential for someone with DM amyotrophy?
cauda equina syndrome, guillain barre syndrome, myositis, myopathy, structural plexus lesion, infections, autoimmune or inflammatory conditions and an EMG or NCS can confirm the diagnosis.
best way to prevent diabetic foot ulcers?
wearing well fitting diabetic footwear, good foot hygiene, and avoiding injury.
treatment options for diabetic peripheral neuropathy?
antidepressants (amitriptyline, duloxetine)
anticonvulsants (pregabalin or valproic acid)
tropical capsaicin cream alpha lipoic acid transcutaneous
electrical nerve stimulation TENS
lidocaine patch
symmetrical sensory neuropathy that affects both distal lower extremities with loss of vibraotry sensation and proprioception and pain in extremities and decreased or absent ankle reflexes
diabetic peripheral neuropathy
what helps with diabetic peripheral neuropathy
tighter glycemic control may help prevent it
side effects of pregabalin
dizziness, somnolence, and confusion seen at higher doses of drug
what is diabetic nephropathy?
albuminuria >300 mg/day or >300 mg/g creatinine on random urine sample.
how to treat diabetic nephropathy?
strict glycemic control and good blood pressure control (goal BP <140/90) and need to RAS inhibition via ACEi or ARB
what does ACE i commonly do after starting to GFR?
can reduce renal capillary pressure (due to greater relaxation of the efferent arteriole) see possible rise in serum K from reduced levels of aldosterone. Can cause an initial decrease in GFR
what is our acceptable change in GFR and Cr change after starting a ACEi with someone who has diabetic nephropathy?
rise of serum Cr of 30-35% from baseline is acceptable and should not cause discontinuation therapy.
what is our acceptable change in K after starting an ACEi or ARB?
Moderate elevations of serum K (5.1-5.5) above normal should lead to dose reductions. Severe elevations that cannot be managed by diuretics mean ACEi should be discontinued.
when to recheck BMP after starting a ACEi or arb
check in 2 weeks and if slight elevation but within our 30-35% change and no hyperkalemia recheck in another 2-3 weeks.
in treatment of DKA what is core therapies of treatment
focus on fluid and electrolyte management with IV insulin and correction of precipitating causes
What are the deficits in pts who present in DKA : IVF K
3-6 L fluid down so tx: NS IVF for 1-2 to expand intravascular volume and improve tissue perfusion. After fluid repletion depends on pt hemodynamic status and sodium level NS is recommended for low Na levels and 1/2 NS given to pts with normal or high Na at presentation. Serum K is high or normal at presentation but they have a total body deficit. So 20-30 mEq of K is added to each liter of IVF to maintain serum K of 4-5 Only hold Na when K >5.2
After pt who presents with DKA has been on IVFs and insulin and their glucose is <200-250 what to do?
give D5 1/2 NS because you want to give dextrose to keep them from getting hypoglycemic as you continue the insulin gtt to help see the resolution of ketosis.
Management of DKA
Resolution of DKA is defined by:
Glucose <200
no anion gap
bicarb is >15
and patient is able to reliably eat and corrected the precipitating factor
intense diabetic control (A1c) provides what benefit?
What does it not do?
A1c decrases risk for microvascular complications (retinopathy, nephropathy) but doesn’t reduce risk of ASCVD esp in those with longstanding DM2.
Some meds can reduce cardiovascular risk: emphagliflozin, canagliflozin, liraglutide, and semaglutide).
Diabetic food ulcers >2 cm are likely to
extend to bone and cause osteomyelitis
acute osteomyelitis presentation
see tenderness, warmth, erythema and swelling and systemic symptoms esp if >2 weeks
see elevated ESR or CRP.
Plain radiographs don’t show acute osteomyeltiis (cortical erions or periosteal elevation or sclerosis for 10-14 days)
Thus MRI is preferred for osteomyelitis but if there’s fracture of Charcot joint it may pick that up too. It can also be negative in pts who have PAD due to lack of blood flow.
