Levent Tekin

Comparison of Quality of Life and Functionality in Patients with Traumatic Unilateral below Knee Amputation and Salvage Surgery

The aim of this study was to compare the functionality during daily activities and quality of life of patients with transtibial amputation vs. salvage surgery after severe lower limb trauma. Ten patients with unilateral below knee amputation and nine patients with salvage surgery after severe lower limb trauma were enrolled. Functional Ambulation Scale (FAS), Visual Analogue Scale (VAS), Short Form 36 (SF-36) Energy Expenditure Index (EEI), 6-Minute Walking Test (6MWT) and 10-Meter Walking Test (10MWT) were used for the evaluation of subjects. Patients in the salvage group were also evaluated radiologically with Graves radiological assessment method and Freiburg ankle scoring system. All patients were classified as grade 5 according to FAS. All SF-36 subgroup values were higher in the amputation group whereas only those of general health and vitality reached statistical significance (p < 0.05). The visual analogue scale (VAS) has been used to assess the efficacy of pain management. Mean VAS scores were found to be statistically higher in the salvage group (p < 0.005). Reoperation rates were one in 10 amputee and six in nine salvage patients. Mean Freiburg ankle scores of the patients in the salvage group were 55.33 ± 15.51 which was consistent with moderate functionality. According to Graves radiological assessment; four patients had grade 3 degeneration, four had grade 2 and one had grade 1 degeneration in the ankle joints. Mean EEI values, 6-MWT and 10-MWT results were not significantly different between the groups (p values > 0.05). Although amputation still remains as the last resort both for patients and the physicians, our results demonstrated that reoperation rates, quality of life (general health and vitality) and pain scores were better in amputee patients.

Quality of Life and Functionality of Patients With Heel Reconstruction After Landmine Explosions

Landmine injuries cause extensive soft and bony tissue loss of the weight‐bearing areas, particularly the heel. Reconstruction of these injuries is challenging, and there are no studies that report long‐term functional results.

Sonographic diagnosis of recurrent peroneal tendon subluxation.

SummaryA case of recurrent peroneal tendon subluxation is reported. Dynamic ultrasonography is the best imaging modality in the diagnosis of peroneal tendon subluxation.ZusammenfassungEs wird über einen Fall rezidivierender Subluxation der Peronealsehnen berichtet. Dynamischer Ultraschall ist das beste bildgebende Verfahren zur Diagnose von rezidivierender Subluxation der Peronäus Sehne.

Calcaneal spur in an 18-month-old boy.

steroids. Chronic dry cough results from ischaemia of the cough receptors (5). Hoarseness is yet another clue for GCA. Male gender, smoking history, and atherosclerosis are risk factors predictive of strokes in patients with GCA. (6). Brainstem strokes generally occur within 2 to 3 months of the non-specific symptom onset (1, 7). GCA patients without prominent systemic symptoms and inflammatory markers are more prone to ischaemic cranial complications (8). This is related to lower angiogenesis and lower levels of vascular endothelial growth factor (VEGF) genes (9). VEGF gene polymorphisms seem to increase the susceptibility to severe ischaemic complications of GCA (10). Biopsy-proven GCA patients with severe occlusive disease (patients with permanent visual loss, stroke, or occlusive disease in the upper extremities) had genotypes associated with lower circulating VEGF levels in vivo and a reduced VEGF transcription (10). This evidence suggests that inflammationinduced angiogenic activity may counteract the development of severe ischaemic complications. A high index of suspicion for GCAmust be maintained in elderly patients presenting with stroke, along with symptoms such as cough, hoarseness, episodic diplopia, occipital headaches, and unexplained elevation in ALP.

Stroke due to anemia after severe menstrual bleeding caused by a uterine myoma: the title is self-explanatory

To the Editor,Cerebral infarction results from acute impairment of oxy-genated blood flow either due to a thrombotic or embolicocclusion. Aside from several likely contributing factors[1], anemia is an overlooked risk factor for cerebralinfarction. Although the relationship between anemia andcerebral infarction has not been well established, severalresearchers reported an association between these twoconditions [2–4].Likewise, we report a patient who had acute cerebralinfarction associated with severe anemia following severeblood loss due to a uterine myoma.A 43-year-old woman was admitted for a sudden onsetof weakness on her left side. Her medical history did notdisclose any risk factor like systemic hypertension, vas-cular malformation, coagulopathy, hyperlipidemia, smok-ing, diabetes mellitus, prior stroke history or positivefamily history. Her cardiac examination including elec-trocardiography and echocardiography was also normal.The laboratory findings were as follows: hemoglobin (Hb):5.7 g/dL (12.8 g/dL 1 month ago), hematocrit (Hct): 21.0,serum iron: 11.9 mg/dL (50–150) and platelet count:594,000/lL. Cranial magnetic resonance imaging (MRI)showed an infarction in the middle cerebral artery suppliedarea (Fig. 1). Overall, the patient was diagnosed to have anischemic cerebral infarction associated with severe anemia.Thereafter, she was given anti-thrombolytic treatment andblood transfusion twice for anemia. Further evaluationsregarding etiology were not contributory except hypo-chromic microcytic anemia. On detailed questioning, shedeclared that her complaints started within the 2 days aftera major bleeding during menstruation. She added that sheusually had similar menstrual bleedings before as well.Upon consultation to the gynecology department, she wasdiagnosed with a huge uterine myoma. She was thenscheduled for hysterectomy in a week after hemodynamicstabilization. After a 2-week rehabilitation program, thepatient discharged was almost independent in her dailyliving.In the previous literature, there are a few anecdotalreports on the association between bleeding, anemia andcerebral infarction [2–4]. Although the relationship amongthem was unclear, Akins et al. [5] presented patients withsevere iron deficiency anemia in whom reactive thrombo-cytosis led to thrombus formation and thus cerebralinfarction. Likewise, Kim et al. [6] also consideredbleeding and subsequent anemia to be a precipitant forcerebral infarction. In that study, they have also reportedthrombocytosis, especially in patients with chronic irondeficiency anemia. In another study whereby patients withanemia—due to acute blood loss—but without iron defi-ciency were enrolled, Tsai et al. [2] mentioned that acuteanemia could induce cerebral blood flow insufficiency anddecreased oxygen-carrying capacity, with an eventual tis-sue hypoxia especially at the most vulnerable regions.Selective decrease in hematocrit has also been reported to