TRANSMETATARSAL AMPUTATION FOR INFECTION OR GANGRENE IN PATIENTS WITH DIABETES MELLITUS

1949 ◽  
Vol 130 (4) ◽  
pp. 826-842 ◽  
Author(s):  
Leland S. McKittrick ◽  
John B. McKittrick ◽  
Thomas S. Risley
2000 ◽  
Vol 90 (1) ◽  
pp. 18-23 ◽  
Author(s):  
VE Kelly ◽  
MJ Mueller ◽  
DR Sinacore

High plantar pressures contribute to skin breakdown in patients with diabetes mellitus and peripheral neuropathy. The primary purpose of this study was to determine the point during the stance phase of walking that corresponds with forefoot peak plantar pressures. Results indicate that peak plantar pressures occurred at 80% +/- 5% of the stance phase of gait in subjects with diabetes and transmetatarsal amputation, as well as in control subjects. Improved methods of footwear design or walking strategies proposed to patients should focus on the demands of the foot during the late stance phase of walking in order to increase available weightbearing area or to decrease forces, which will minimize plantar pressures and reduce trauma to the neuropathic foot.


1993 ◽  
Vol 83 (2) ◽  
pp. 91-95 ◽  
Author(s):  
BI Rosenblum ◽  
DV Freeman

Recurrent ulcerations may develop following transmetatarsal amputation in patients with diabetes mellitus. In many cases, these ulcerations require surgical intervention to achieve healing, especially in situations where conservative care has not been effective. These procedures range from the local resection of bone to skin grafting and flap techniques to successfully heal the wound. The ultimate goal of any surgical intervention is to prevent a more proximal amputation.


Author(s):  
Bruce R. Pachter

Diabetes mellitus is one of the commonest causes of neuropathy. Diabetic neuropathy is a heterogeneous group of neuropathic disorders to which patients with diabetes mellitus are susceptible; more than one kind of neuropathy can frequently occur in the same individual. Abnormalities are also known to occur in nearly every anatomic subdivision of the eye in diabetic patients. Oculomotor palsy appears to be common in diabetes mellitus for their occurrence in isolation to suggest diabetes. Nerves to the external ocular muscles are most commonly affected, particularly the oculomotor or third cranial nerve. The third nerve palsy of diabetes is characteristic, being of sudden onset, accompanied by orbital and retro-orbital pain, often associated with complete involvement of the external ocular muscles innervated by the nerve. While the human and experimental animal literature is replete with studies on the peripheral nerves in diabetes mellitus, there is but a paucity of reported studies dealing with the oculomotor nerves and their associated extraocular muscles (EOMs).


1988 ◽  
Vol 59 (02) ◽  
pp. 269-272 ◽  
Author(s):  
M B Grant ◽  
C Guay ◽  
R Lottenberg

SummaryDesmopressin acetate administration markedly stimulates release of tissue plasminogen activator (t-PA) from vascular endothelial cells. The mechanism for this effect is unknown. Because infusion of epinephrine has been shown to increase t-PA levels, we examined the role of endogenous catecholamine mediation of t-PA release by desmopressin. Intravenous desmopressin acetate (0.3 μg/kg) was infused over 30 min in 9 controls and 11 subjects with diabetes mellitus, a condition associated with abnormalities of the fibrinolytic system. Plasma was collected in the supine, overnight fasted state at 15 min intervals (0-60 min) for measurement of t-PA activity, t-PA antigen and fractionated catecholamines. t-PA activity peaked at 30-45 min and subsequently decreased. The norepinephrine levels paralleled the t-PA activity. t-PA activity increased 10-fold from 0.14 ± .12 to 1.49 ± 0.79 IU/ml (Mean ± SD) and plasma norepinephrine increased 2- fold from 426 ± 90 to 780 ± 292 pg/ml. However, epinephrine and dopamine levels did not change significantly. The response to desmopressin of control and diabetic subjects was not shown to differ and their data were combined. We conclude that desmopressin increases plasma norepinephrine in addition to t-PA and that the parallel time course of change suggests a possible role for norepinephrine in mediating endothelial cell t-PA release.


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