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Keio Journal of Medicine 2008-Dec

Deep venous thrombosis in stroke patients during rehabilitation phase.

Samo registrirani uporabniki lahko prevajajo članke
Prijava / prijava
Povezava se shrani v odložišče
Yukihiro Hara

Ključne besede

Povzetek

OBJECTIVE

The purpose of this study was to examine the incidence, factors, and effects of antiplatelet and anticoagulant agents on sub-acute and chronic ischemic stroke patients during the rehabilitation phase for rates of deep venous thrombosis (DVT) from the perspective for rehabilitation medicine.

METHODS

In this study of 272 patients undergoing rehabilitation for completed cerebral infarction, multiple circumference measurements of calf and thigh along with presence or absence of symptoms (congestion, swelling, skin redness, warmth, pain, pigmentation, fever and/or Homan sign or Luck's sign) documented in the physical examination were recorded in all patients. Patients with these symptoms suggestive of DVT were included for D-dimer assay and venous duplex ultrasonography to confirm presence of DVT.

RESULTS

DVT was documented in 24 patients (8.8%), most of whom displayed distal DVT on the hemiparetic side. A significant association was seen between occurrence of DVT and more severe lower limb paresis, manifesting as gait disturbance, severe calf muscle spasticity, use of ankle-foot orthosis (AFO). A significant increase in development of DVT was associated with severe spasticity in hemiparetic calf muscles (odds ratio (OR) 28.2; 95% confidence interval (CI), 6.9-113.5). Cilostazol seemed to be the only effective antiplatelet drug for preventing DVT in cerebral infarction patients.

CONCLUSIONS

Incidence of DVT in the rehabilitation phase following stroke was not low, which was predominant as distal DVT on the hemiparetic side. Lower limb paresis, gait disturbance, calf muscle spasticity and use of AFO contributed to occurrence of DVT. It is likely that micro-injuries in the venous endothelium due to spasticity and AFO might cause DVT. Cilostazol seems effective for protecting against venous endothelial damage following DVT.

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