Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Ravi K. Bobba is active.

Publication


Featured researches published by Ravi K. Bobba.


Clinical Infectious Diseases | 2005

Neuroimaging as a Guide to Predict Outcomes for Patients with Coccidioidal Meningitis

Edward L. Arsura; Royce Johnson; James Penrose; Kenneth Stewart; William B. Kilgore; Chakradhar M. Reddy; Ravi K. Bobba

Sixty-two patients with coccidioidal meningitis underwent neuroimaging. Magnetic resonance imaging detected neuroimaging abnormalities in 76% of patients, and computed tomography scanning detected neuroimaging abnormalities in 41.6%. The most common abnormal neuroimaging findings were hydrocephalus (51.6%), basilar meningitis (46.8%), and cerebral infarction (38.7%). Significantly elevated mortality rates were associated with hydrocephalus and hydrocephalus coexisting with infarction. Basilar meningitis did not influence outcome. Patients without neuroimaging abnormalities had a mortality rate of 7.7%.


Annals of Clinical Microbiology and Antimicrobials | 2004

Emphysematous cystitis: An unusual disease of the Genito-Urinary system suspected on imaging

Ravi K. Bobba; Edward L. Arsura; Pawanjit S Sarna; Amar K. Sawh

Emphysematous cystitis is a rare disease entity caused by gas fermenting bacterial and fungal pathogens. Clinical symptoms are nonspecific and diagnostic clues often arise from the unanticipated imaging findings. We report a case of 52-year-old male who presented with fever, dysuria and gross hematuria who was found to have emphysematous cystitis.


Digestive Diseases and Sciences | 2005

Abdominal pain secondary to pylephlebitis: an uncommon disease of the portal venous system, treated with local thrombolytic therapy.

Rathnakara Sherigar; Khalil A. Amir; Ravi K. Bobba; Edward L. Arsura; Narain Srinivas

Pylephlebitis is a rare complication of intraabdominal inflammatory processes that carries an elevated mortality rate. Even in the modern era, diagnosis and treatment are difficult because of the nonspecific nature of clinical signs and symptoms and laboratory studies. We present a patient with pylephlebitis who had rapid resolution of symptoms after administration alteplase (tPA). The outcome of this uncommon entity can be improved with a high index of clinical suspicion, better imaging modalities, and interventional radiology techniques.


Digestive Diseases and Sciences | 2005

Hepatic portal and mesenteric vein gas as a late complication of percutaneous endoscopic gastrostomy tube placement in an elderly patient.

Ravi K. Bobba; Edward L. Arsura

Hepatic portomesenteric venous gas (HPVG) most often represents an ominous clinical finding. The presentation is usually consistent with an acute abdomen but at times vague abdominal symptoms and nonspecific laboratory predominate. The occurrence of HPVG as a late complication from percutaneous endoscopic gastrostomy (PEG) tube placement is a previously unreported event. PEG is a frequently performed procedure and the clinician should be aware of the significance of HPVG in a patient with recent PEG.


Journal of the American Geriatrics Society | 2007

ACUTE ABDOMINAL AORTIC THROMBOSIS AS A COMPLICATION OF THE HEIMLICH MANEUVER

Thomas J. Martin; Ravi K. Bobba; Rosemarie Metzger; Macrea Madalina; Madhavi Bollu; Bharatbhai G. Patel; Mehdi M. Kazemi

1. Shaw PJ, Walls TJ, Newman PK et al. Hashimoto’s encephalopathy: A steroidresponsive disorder associated with high anti-thyroid antibody titers-report of 5 cases. Neurology 1991;41:228–233. 2. Azuma T, Uemici T, Funaucghi M et al. Myelopathy associated with Hashimoto’s disease. J Neurol Neurosurg Psychiatry 2000;68:679–683. 3. Chong JY, Rowland LP, Utiger RD. Hashimoto encephalopathy: Syndrome or myth? Arch Neurol 2003;60:164–171. 4. Ferracci F, Bertiato G, Moretto G. Hashimoto’s encephalopathy: Epidemiologic data and pathogenetic considerations. J Neurol Sci 2004;217:165–168. 5. Ferlazzo E, Raffaele M, Mazzu I et al. Recurrent status epilepticus as the main feature of Hashimoto’s encephalopathy. Epilepsy Behav 2006;8:328–330. 6. Nolte KW, Unbehaun A, Sieker H et al. Hashimoto encephalopathy: A brainstem vasculitis? Neurology 2000;54:769–770. 7. Duffey P, Yee S, Reid IN et al. Hashimoto’s encephalopathy: Postmortem findings after fatal status epilepticus. Neurology 2003;61:1124–1126. 8. Doherty CP, Schlossmacher M, Torres N et al. Hashimoto’s encephalopathy mimicking Creutzfeldt-Jakob disease: Brain biopsy findings. J Neurol Neurosurg Psychiatry 2002;73:601–602. 9. Perrot X, Giraud P, Biacabe AG et al. Hashimoto’s encephalopathy: An anatomicoclinical observation. Rev Neurol 2002;158:461–466. 10. Mahad D J, Staugaitis S, Ruggieri P et al. Steroid-responsive encephalopathy associated with autoimmune thyroiditis and primary CNS demyelination. J Neurol Sci 2005;228:3–5.


The American Journal of the Medical Sciences | 2012

Skin Metastases in Non-small Cell Lung Cancer

Ravi K. Bobba; Donald C. Doll; Michael C. Perry; Jamie L. Odem

Abstract: Skin metastasis associated with lung cancer is an uncommon manifestation and usually portends an aggressive clinical course. It can be either synchronous with the underlying malignancy or be the sign of recurrence. Solitary metastases can be treated with surgical resection or radiation therapy, but multiple lesions are usually treated with palliative chemotherapy. With standard platinum-based doublet regimens, treatment results are usually poor. With the advent of newer agents like pemetrexed, bevacizumab and erlotinib, perhaps results may improve with ongoing clinical trials.


Journal of the American Geriatrics Society | 2009

GELASTIC PRESYNCOPE: AN UNUSUAL MANIFESTATION IN AN ELDERLY PATIENT

Dakshinamurty Gullapalli; Zenon A. Belak; Andres Marte-Grau; Madhavi Bollu; Pavan Reddy; Ravi K. Bobba

CASE REPORT A 67-year-old man was seen in consultation for the complaint of near blackout spells with laughter. The first episode occurred while listening to a radio program while driving, when his laughing heavily resulted in blurring vision, darkening of visual field, feeling faint, and sensation of imminent loss of consciousness. He slowed his vehicle and pulled off the road, and the symptoms soon resolved. He denied complete loss of consciousness, uncontrolled movement of limbs, bowel or bladder incontinence, headache, or other associated symptoms. Since this index episode, patient reports recurrent episodes of near loss of consciousness associated with vigorous laughing. Episodes last only a few seconds. He had similar symptoms, but of lesser severity, in relation to straining during defecation and micturition. The patient denied any palpitations, irregular heartbeat, chronic cough, chest pain, shortness of breath, nausea or vomiting, diarrhea, other systemic or constitutional symptoms, having had stroke in the past, any history of seizures, or any sleep disturbances, including any symptoms suggestive of narcolepsy or cataplexy. His medical history was significant for diabetes mellitus, hypertension, and prolonged posttraumatic disorder, which were stable. The patient was evaluated using magnetic resonance imaging and a magnetic resonance angiogram of the brain, which showed only mild periventricular white matter changes that were nonspecific. Carotid Doppler studies were unremarkable. Chest X-rays were normal. No further diagnostic investigation was pursued because behavioral modification of avoiding vigorous prolonged laughter resolved his symptoms completely. DISCUSSION Gelastic presyncope or syncope is a relatively uncommon type of neurally mediated event with a drop in systemic vascular resistance due to arterial dilation in the setting of a relative or absolute bradycardia. During prolonged laughter, there is repetitive Valsalva effect with reduced venous return secondary to increased intrathoracic pressure with associated systemic arterial dilatation and bradycardia resulting in reduced cardiac output and cerebral hypoperfusion. If the Valsalva effort is not aborted during the presyncopal phase, it is likely that it will culminate in a syncopal episode. This mechanism is similar to that seen with cough syncope. In addition, emotional factors and cerebral vasoconstriction secondary to systemic hypocapnia could be contributing to the syncope in this situation. This patient also had presyncopal sensations to straining from defecation and urination, suggesting Valsalva effect as the most likely mechanism. Laughter or gelastic syncope can potentially be misdiagnosed as cataplexy related to laughter. There have been only a few case reports of laughter syncope previously reported, mostly in the elderly population, in healthy adults and people predisposed to dysautonomia. Possible contribution of dysautonomic neuropathy secondary to diabetes mellitus can not be excluded in the current patient. A more-serious underlying mechanism of severe vascular disease involving the brachiocephalic trunk was noted to be the mechanism in the first reported case of laughter syncope. Syncope resolved after percutaneous angioplasty. Falls in elderly people can lead to devastating consequences, and hence it is essential to diagnose and prevent syncope in this age group. Beta-blockers and midodrine were noted to have beneficial effects in controlling symptoms in one described case of neurally mediated syncope. Behavioral modification may be the best initial approach before exposing the patients to medications.


European Journal of Neurology | 2006

Impact of the duration of antiplatelet therapy after vertebrobasilar artery stent placement

R. Sherigar; Ravi K. Bobba; Edward L. Arsura

1. Prusiner SB. Genetic and infectious prion diseases. Archives of Neurology 1993; 50: 1129–1153. 2. Aitken A, Baxter H, Dubois T, et al. Specificity of 14-3-3 isoform dimer interactions and phosphorylation. Biochemical Society Transactions 2002; 30: 351–360. 3. Brandel JP. Clinical aspects of human spongiform encephalopathies, with the exception of iatrogenic forms. Biomedicine and Pharmacotherapy 1999; 53: 14–18. 4. Beaudry P, Cohen P, Brandel JP, et al. 14-3-3 protein, neuron-specific enolase, and S-100 protein in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease. Dementia and Geriatric Cognitive Disorders 1999; 10: 40–46. 5. Peoc’h K, Beaudry P, Laupretre N, et al. CSF detection of the 14-3-3 protein in unselected patients with dementia. Neurology 2002; 12: 509–510.


Southern Medical Journal | 2004

Cognitive decline in an elderly hospitalized patient with primary leptomeningeal melanomatosis

Ravi K. Bobba; Edward L. Arsura

Delirium is one of the most common disorders in hospitalized patients. The authors present the case of an elderly male patient with postoperative cognitive decline that did not resolve with the conventional treatment. The diagnosis was only established on autopsy. A 75-year-old man was evaluated after a fall. Initial evaluation revealed voluntary guarding in the right epigastric region, and free air was detected under the right hemidiaphragm on abdominal radiography. An exploratory laparotomy revealed a perforation that had apparently sealed off. After surgery, he had initial improvement toward baseline; however, after several days, his postoperative course was complicated by a progressive deterioration in mental status, recurrent seizures, and aspiration pneumonia. Computed tomographic scan of the brain showed communicating hydrocephalus. Examination of the cerebrospinal fluid revealed an elevated opening pressure and elevated protein. His mental status continued to deteriorate, and he died. Autopsy revealed the pathologic diagnosis of primary leptomeningeal melanomatosis.


The American Journal of the Medical Sciences | 2009

New onset atrial fibrillation developing in medical inpatients.

Sydney X. Chen; Edward L. Arsura; Khalil A. Amir; Ravi K. Bobba

Background:The outcome of patients who develop new onset atrial fibrillation (AF) after admission to an Internal Medicine service for acute medical illnesses is unknown. Methods:In a retrospective review, we compared patients in the study group: patients who were admitted to hospital for acute medical illnesses and subsequently developed new onset AF during hospitalization, with a control group 1: patients whose admitting diagnosis was new onset AF and a control group 2: patients who were admitted for acute medical illnesses and never developed AF. We analyzed clinical characteristics and all-cause mortality rate during the first 30 days, 6 months, and 1 year after admission. Results:The 1-year mortality rates in study group were significantly higher than control group 1 (62% versus 8%, P < 0.001) and control group 2 (62% versus 29%, P < 0.05). These results suggest that AF and acute medical illness both are risk factors for increased mortality. The odds ratios were 4.05 (P = 0.023) and 18.33 (P = 0.001) for AF and acute medical illnesses, respectively, indicating that acute medical illness is the better predictor for mortality. Troponin I levels were elevated in 46% of patients in study group versus 12% in control group 1 and 42% in control group 2 (P < 0.05). Conclusions:Medical inpatients who develop new onset AF during hospitalization for acute medical illnesses have an increased mortality when compared with patients who were admitted solely for new onset AF. Acute medical illness rather than AF plays a more important role on the increased mortality in this subset of patient population.

Collaboration


Dive into the Ravi K. Bobba's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Mark E. Williams

Beth Israel Deaconess Medical Center

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge