Assessing in-hospital mortality and predictors in Patients with contrast-induced nephropathy Following primary percutaneous coronary Intervention.

BACKGROUND: The contrast-induced nephropathy (CIN) is a common complication of primary percutaneous coronary intervention (PCI) it has been reported to be associated with an increased risk of mortality. The study reported the in-hospital mortality among patients who developed CIN after primary PCI. METHODS: This descriptive cross-sectional study was conducted on a sample of consecutive who developed CIN after primary PCI at a tertiary care cardiac hospital in Karachi, Pakistan. The CIN was defined as either a relative increase of 25% or an absolute increase of 0.5 mg/dL in post -procedure serum creatinine within 72 hours. The in-hospital mortality status was recorded and clinical and demographic predictors of in-hospital mortality were identified with the help of binary logistic regression analysis. RESULTS: In the study sample of 402 patients, 74.1% (298) were male and the mean age of the study sample was 59.4±11.5 years. The in-hospital mortality rate was 9.7% (39). On multivar iable analysis, an increased risk of mortality was found to be independently associated with inferior wall myocardial infarction (IWMI) with right ventricular (RV) infarction, intra-procedure arrhythmias, and pump failure with an adjusted odds ratio of 3.63 [95% CI: 1.31-10.08; p=0.013], 5.53 [95% CI: 1.39-22.06; p=0.015], and 8.94 [95% CI: 3.99-20.02; p<0.001], respectively. CONCLUSIONS: In conclusion, there is a high rate of mortality for patients who develop CIN after primary PCI, and the risk of mortality is further aggravated by the presence of IWMI with RV infarction, intra-procedure arrhythmias, and pump failure.

A rare case of renal infarction due to heroin and amphetamine abuse: case report.

BACKGROUND: Renal infarctions as a result of recreational drug use are rare and are commonly associated with cocaine use. Although amphetamines have a similar mechanism of action as cocaine, there are few reports linking them to ischemic events, and only one to renal infarction. Similarly, few reports link heroin use with infarcts, but never in the kidney. Although uncommon, several mechanisms have been implicated in heroin and amphetamine-induced infarction, including vasculopathy, vasculitis and the activation of the coagulation cascade. CASE PRESENTATION: 47-year-old female with a past medical history of non-intravenous heroin and amphetamine abuse, chronic obstructive pulmonary disease, hypertension, hyperlipidemia presented with right lower extremity swelling and rash, which was diagnosed as cellulitis and treated appropriately. Incidentally, the patient was found to have an acute kidney injury and further workup identified multiple renal infarcts in the right kidney. The patient had no past medical history of clotting disorders. Blood culture and urine cultures were sterile; autoimmune and hypercoagulable workup were negative. Urinalysis was unremarkable. Urine toxicology was only positive for opiates and amphetamines, which were thought to be the most likely cause of the renal infarct. Patient was lost to outpatient follow up due to noncompliance, but returned to the hospital for re-emergence of her cellulitis, during which no new infarcts were discovered, and the previous renal infarct had scarred over. CONCLUSION: There are very few reports of heroin and amphetamine-induced infarctions. This case report describes a rare but important complication of heroin/amphetamine abuse that could be easily overlooked.

Bilateral macular infarction after gemcitabine and carboplatin chemotherapy.

PURPOSE: To report a case of macular infarction after doublet chemotherapy with gemcitabine and carboplatin. METHODS: A middle-aged lady presenting with bilateral macular infarction post-chemotherapy for metastatic cervical malignancy was investigated for thromboembolic risks and treated. RESULTS: The macular perfusion and edema improved with control of hypertension and treatment with pentoxifylline. Visual improvement was satisfactory, and the possible associated risk such as hypertension was noted. CONCLUSION: This case underscores the need for active screening of patients on chemotherapy with gemcitabine and carboplatin for retinal vascular occlusive changes when hypertension is associated.

Taking varenicline for smoking cessation: A rare cause of pulmonary thromboembolism with infarction.

Varenicline (Champix®, Chantix®) is a partial agonist of the α4ß2 nicotinic acetylcholine receptor (nAChR) and a full agonist of the α7 nAChR. It has been used for smoking cessation since 2006. Varenicline has been associated with adverse cardiovascular (CV) events, including myocardial infarction, which may be caused by activation of the α7 nAChR receptor that in turn stimulates parasympathetic output from the brainstem to the heart, release of catecholamines, and has a prothrombotic effect. However, among the adverse CV events, the issue related to the varenicline-induced pulmonary thromboembolism (PTE) has not being addressed. We report a case of PTE with pulmonary infarction presenting as right flank pain that resulted from the use of varenicline (the total score of adverse drug reaction probability scale, 6; probable association between varenicline and pulmonary PTE) in a patient without underlying CV disease and in whom low probability of PTE (Wells score was zero) was identified.

Acute Bilateral Renal and Splenic Infarctions Occurring during Chemotherapy for Lung Cancer.

We herein report a rare case of acute bilateral renal and splenic infarctions occurring during chemotherapy for lung cancer. A 60-year-old man presented with acute and intensive upper abdominal and back pain during chemotherapy with cisplatin and etoposide for lung cancer. Contrast-enhanced computed tomography (CT) revealed bilateral renal and splenic infarctions. After the administration of unfractionated heparin his pain was relieved with a clearance of the infarctions in the CT findings and a recovery of renal dysfunction. Enhanced coagulation by lung cancer and arterial ischemia by chemotherapy may therefore contribute to the development of these infarctions.

Ocular dysmotility after intra-arterial chemotherapy for retinoblastoma.

We report the case of a 15-month-old boy with retinoblastoma who developed exotropia secondary to a right medial rectus infarct after intra-arterial chemotherapy. He had unilateral sporadic group C tumor (International Classification of Retinoblastoma) and was treated with intra-arterial melphalan. One week after the first session of intra-ophthalmic arterial melphalan chemotherapy, he was noted to have orbital congestion, exotropia, and right adduction limitation. Magnetic resonance imaging was suggestive of a right medial rectus infarct. The tumor showed a good response to intra-arterial chemotherapy but the exotropia persisted.

18F-FDG PET imaging in a patient with late omental infarction after treatment of pancreatic adenocarcinoma.

We report a case of late omental infarction visualized by F-FDG PET/CT during follow-up for pancreatic adenocarcinoma. The 65-year-old patient was referred for imaging 8 months after pancreaticoduodenectomy and 2 months after completion of a course of chemotherapy. PET/CT showed an FDG-avid omental lesion that suggested peritoneal carcinomatosis. The appearance and evolution at follow-up studies confirmed the diagnosis of omental infarction, a rare complication of pancreatic surgery. This case revealed the possibility of late FDG uptake in omental infarction.

Non-invasive monitoring of tumor-vessel infarction by retargeted truncated tissue factor tTF-NGR using multi-modal imaging.

The fusion protein tTF-NGR consists of the extracellular domain of the thrombogenic human tissue factor (truncated tissue factor, tTF) and the peptide GNGRAHA (NGR), a ligand of the surface protein CD13 (aminopeptidase N), upregulated on endothelial cells of tumor vessels. tTF-NGR preferentially activates blood coagulation within tumor vasculature, resulting in tumor vessel infarction and subsequent tumor growth retardation/regression. The anti-vascular mechanism of the tTF-NGR therapy approach was verified by quantifying the reduced tumor blood-perfusion with contrast-enhanced ultrasound, the reduced relative tumor blood volume by ultrasmall superparamagnetic iron oxide-enhanced magnetic resonance imaging, and by in vivo-evaluation of hemorrhagic bleeding with fluorescent biomarkers (AngioSense(680)) in fluorescence reflectance imaging. The accumulation of tTF-NGR within the tumor was proven by visualizing the distribution of the iodine-123-labelled protein by single-photon emission computed tomography. Use of these multi-modal vascular and molecular imaging tools helped to assess the therapeutic effect even at real time and to detect non-responding tumors directly after the first tTF-NGR treatment. This emphasizes the importance of imaging within clinical studies with tTF-NGR. The imaging techniques as used here have applicability within a wider scope of therapeutic regimes interfering with tumor vasculature. Some even are useful to obtain predictive biosignals in personalized cancer treatment.

Hemorrhagic retinal infarction due to inadvertent overdose of cefuroxime in cases of complicated cataract surgery: retrospective case series.

PURPOSE: To present 4 patients that developed hemorrhagic retinal infarction attributable to inadvertent overdose of cefuroxime after cataract surgery. DESIGN: Case series. SUBJECTS AND METHODS: Surgery in 4 patients was complicated-the posterior capsule was absent or torn-and anterior vitrectomy was performed. Cefuroxime was inadvertently injected at a dose higher than recommended in all 4 cases. RESULTS: Case 1 had hemorrhage in the central and inferior retinal regions, as well as optic atrophy. Case 2 had hemorrhage in the peripapillary and macular regions, as well as optic atrophy. Case 3 had hemorrhage in the peripapillary and inferior retinal regions, as well as macular pucker attributable to fibrovascular formation in the central retinal region. Case 4 had hemorrhage in the peripapillary, macular, and inferior retinal regions. The cefuroxime doses administered to the presented patients were much higher than reported in other cases and resulted in a higher concentration in the vitreous. Consequently, the severity of toxicity was much higher than in other reported cases of cefuroxime-induced toxicity. CONCLUSION: In cases of intracameral cefuroxime overdose, hemorrhagic retinal infarction can develop after cataract surgery.

Spinal infarction related to the adjuvant chemotherapy for surgically resected non-small cell lung cancer: report of a case.

We report the development of spinal infarction during adjuvant chemotherapy with tegafur, gimeracil and oteracil (TS-1) after surgery for lung adenocarcinoma. A 69-year-old female had a left upper lobectomy for pulmonary adenocarcinoma, T2aN0M0. Six weeks after the surgery, tegafur, gimeracil and oteracil were administered orally as adjuvant chemotherapy for 1 year. After 10 months of adjuvant chemotherapy, the patient suddenly showed signs of numbness and weakness in both lower limbs. The patient did not have a previous medical history, and was receiving only tegafur, gimeracil and oteracil with the stomach medication. Neurological findings showed muscle weakness, numbness and a loss of tendon reflex in both lower limbs, as well as bladder and rectal disturbance. Blood tests, brain magnetic resonance imaging and chest computed tomography showed no signs of abnormalities or metastasis. Magnetic resonance imaging of the spine showed a hyperintense lesion between the Th12 and L1 spinal levels by T2-weighted image. A spinal fluid test indicated no abnormalities, and cytological diagnosis was class II. Anti-aquaporin 4, anti-ganglioside and anti-neuronal autoantibodies were all negative. These results indicated that the patient had a spinal infarction, rather than myelitis or paraneoplastic neurological syndrome. The patient was treated with heparin and steroid pulse treatment followed by rehabilitation, and recovered sufficiently to be able to walk using a cane after 2 months. The development of spinal infarction during anti-cancer chemotherapy has not been previously reported. In this case, an association of spinal infarction with the use of adjuvant chemotherapy was strongly indicated due to the lack of abnormalities in coagulability, atherosclerotic lesions and aortic disease.

Old drugs: new complications.

This is a case of acute splenic and bilateral renal infarction in a patient with non-small cell lung carcinoma during chemotherapy with gemcitabine and cisplatin. Till date, bilateral renal infarction following gemcitabine and cisplatin has been reported only once in the past. The case that is being reported has had acute splenic and bilateral renal infarct and has not been reported previously. Splenic and renal infarction should be considered in the differential diagnosis of excruciating abdominal pain and backache in a patient on gemcitabine-based and cisplatin-based chemotherapy.

Renal cortical infarction following treatment with sumatriptan in a kidney allograft recipient.

Renal cortical infarction is a rare cause of acute kidney injury that results from inadequate blood flow to the kidney, most commonly as a consequence of thrombotic or embolic occlusion of the renal artery or profound hypoperfusion. We report the case of a 78-year-old female kidney transplant recipient who developed a migraine headache, took sumatriptan, and soon after developed pain over the allograft and oligoanuric acute kidney injury. Kidney allograft biopsy showed renal cortical infarction. The mechanism of action of sumatriptan involves vasoconstriction, which counters the vasodilatation that is central to the pathogenesis of migraines. This case raises important questions regarding the safety of triptans with calcineurin inhibitors (which also act to vasoconstrict), particularly in elderly patients.

Macular infarction following intravitreal bevacizumab for treatment of central retinal vein occlusion.

Bevacizumab, a monoclonal antibody against vascular endothelial growth factor (VEGF), is widely used for the treatment of macular edema associated with central retinal vein occlusion (CRVO). The authors present a series of three patients with CRVO who suffered apparent macular infarction within weeks of intravitreal administration of bevacizumab. Of the nearly 200 patients undergoing intravitreal injections of bevacizumab for this indication over a surveillance period of 3 years, this event occurred in three patients. This has not been described in the natural history of the disease and is associated with poor visual outcomes.