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Dive into the research topics where Deepak Gunjan is active.

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Featured researches published by Deepak Gunjan.


Digestive and Liver Disease | 2018

Prevalence, predictors and impact of bacterial infection in acute on chronic liver failure patients

Shalimar; Gyanranjan Rout; Shekhar Jadaun; Gyan Ranjan; Saurabh Kedia; Deepak Gunjan; Baibaswata Nayak; Subrat K. Acharya; Ajay Kumar; Arti Kapil

BACKGROUND Acute on chronic liver failure (ACLF) is associated with high short term mortality. We aimed to evaluate the prevalence, predictors and impact of bacterial infection in ACLF. METHODS Consecutive hospitalized patients with cirrhosis and acute decompensation (AD), from January 2011-March 2017, were included. Predictors of survival and infection were assessed. RESULTS 572 patients with cirrhosis and AD were classified into 3 groups - no infection (group 1, n = 190, 33.2%), infection at admission/within 48 h (group 2, n = 298, 52.1%) and infection after 48 h (group 3, n = 84, 14.7%). Higher frequency of organ failures - kidney, brain, circulation and respiratory failure - were seen in groups 2 and 3 as compared with group 1 (P < 0.001 for all). Most common site of infection was lungs, followed by spontaneous bacterial peritonitis and urinary tract infection. The frequency of infection increased with higher ACLF grades. Among ACLF patients, on Cox-proportional multivariate analysis, presence of infection was associated with significantly higher mortality [group 2 (HR 2.93; 95%CI, 1.97-4.38, P < 0.001) and group 3 (HR 1.84; 95%CI, 1.16-2.91, P = 0.009)], as compared with group 1. On multivariate logistic regression analysis, advanced hepatic encephalopathy and elevated total leucocyte count were independently associated with development of infection. CONCLUSIONS Infections are common in ACLF, and associated with poor outcome.


Indian Journal of Gastroenterology | 2018

Alcohol-related acute-on-chronic liver failure—Comparison of various prognostic scores in predicting outcome

Ujjwal Sonika; Shekhar Jadaun; Gyan Ranjan; Gyanranjan Rout; Deepak Gunjan; Saurabh Kedia; Baibaswata Nayak; Shalimar

Background and AimsVarious prognostic scores are available for predicting outcome in acute-on-chronic liver failure (ACLF). We compared the available prognostic models as predictors of outcome in alcohol-related ACLF patients.MethodsAll consecutive patients with alcohol-related ACLF were included. At admission, prognostic indices-acute physiology and chronic health evaluation score (APACHE II), model for end-stage liver disease (MELD), MELD-Na, Maddrey’s discriminant function (DF), age-bilirubin-INR-creatinine (ABIC), and Chronic Liver Failure Consortium (CLIF-C) ACLF score (CLIF-C ACLF) score were calculated. Receiver operator characteristic (ROC) curves were plotted for all prognostic scores with in-hospital, 90-day, and 1-year mortality as outcome.ResultsOf the 171 patients, 170 were males, and grade 1 ACLF in 20 (11.7%), grade 2 in 52 (30.4%), and grade 3 in 99 (57.9%) patients. One hundred and nineteen (69.6%) died in-hospital. The median (IQR) Maddrey’s score, MELD, MELD-Na, ABIC, APACHE II, and CLIF-C ACLF were 87.8 (66.5–123.0), 33.1 (27.6–40.0), 34.4 (29.5–40.0), 8.5 (7.3–9.6), 15 (12–21), and 51.1 (44.1–56.4), respectively. On multivariate Cox regression analysis, independent predictors of in-hospital outcome were presence of hepatic encephalopathy (early HR, 2.078; 95%CI, 1.173–3.682, p = 0.012 and advanced, HR, 2.330; 95% CI, 1.270–4.276, p = 0.006), elevated serum creatinine (HR, 1.140; 95% CI, 1.023–1.270, p = 0.018), and infection at admission (HR, 1.874; 95% CI, 1.160–23.029, p = 0.010). On comparison of ROC curves, APACHE II and CLIF-C ACLF AUROC were significantly higher than MELD, MELD-Na, DF, and ABIC (p < 0.05) for predicting in-hospital, 90-day, and 1-year mortality. The AUROC was highest for APACHE II followed by CLIF-C ACLF (Hanley and McNeil, p = 0.660).ConclusionsAlcohol-related ACLF has high in-hospital mortality. Among the available prognostic scores, CLIF-C ACLF and APACHE II perform best.


Endoscopy | 2018

Endoscopic ultrasonography-guided obliteration of a left inferior phrenic artery pseudoaneurysm in a patient with alcoholic chronic pancreatitis

Deepak Gunjan; Shivanand Gamanagatti; Pramod Kumar Garg

A 43-year-old man who was known to have alcoholic chronic pancreatitis presented with upper gastrointestinal bleeding (UGIB) with shock in September 2016. He was resuscitated with crystalloids and a blood transfusion. He underwent gastroduodenoscopy, colonoscopy, and computed tomographic angiography (CTA), but no source of bleeding was revealed. He had a second episode of UGIB in December 2017. CTA on this occasion revealed contrast extravasation, probably from the left inferior phrenic artery (LIPA) (▶Fig. 1). Digital subtraction angiography (DSA) confirmed the contrast leak from the LIPA (▶Fig. 2) but embolization could not be performed owing to dissection of the artery during wire manipulation. Percutaneous thrombin (500 units) was therefore injected using a trans-splenic approach under Doppler ultrasonography guidance (▶Fig. 3) with subsequent thrombosis of the pseudoaneurysm. The patient re-bled 1 month later and CTA showed a revascularized LIPA pseudoaneurysm. Because of the large size of the pseudoaneurysm and the previously failed DSA, endoscopic ultrasonography (EUS)-guided obliteration was planned. Linear EUS examination from the gastroesophageal junction showed a large pseudoaneurysm (3.6 ×2.3 cm). The pseudoaneurysm was punctured with a 19-gauge needle (Echo-19; Cook India) and 3mL undiluted N-butyl 2-cyanoacrylate glue (NBCA) was injected to completely obliterate the pseudoaneurysm including the feeding vessel (▶Video1). There has been no recurrence of bleeding during the subsequent 9 months of follow-up. Chronic pancreatitis-associated pseudoaneurysmal bleeding is well known. EUS has been reported as being useful both for the diagnosis and embolization of pseudoaneurysms [1]. The present case was unusual in many respects: (i) the involvement of the LIPA is rare with only one published report in chronic pancreatitis and the location of the pseudoaneurysm made it unsuitable for percutaneous intervention [2]; (ii) the pseudoaneurysm was large (>3 cm in size); and (iii) EUS-guided glue injection has been used infrequently. Because of the E-Videos


Endoscopy | 2018

Dislodged hood stuck in submucosal tunnel: retrieval during peroral endoscopic myotomy

Deepak Gunjan; Saransh Jain; Pramod Kumar Garg

A 42-year-old man with type II achalasia cardia underwent peroral endoscopic myotomy (POEM) by posterior approach. The procedure was started using a gastroscope fitted with a conical hood (DH28GR, Fujifilm, Tokyo, Japan). The gastroesophageal junction (GEJ) was tight when the scope reached the lower end during the creation of the submucosal tunnel. The scope was maneuvered to pass beyond the GEJ. However, the hood became stuck at the tight GEJ and slipped off the gastroscope. During an attempt to remove the hood using a rat-tooth forceps, one portion of the hood chipped off (▶Fig. 1). The hood was tightly stuck in the submucosal tunnel and the mucosa prolapsed inside the tunnel (▶Fig. 2). Forceful removal of the hood could have caused mucosal injury. We decided to proceed with myotomy to decrease the pressure in the submucosal tunnel and create more space. Myotomy was continued until we reached the hood and was carefully extended between the muscle and the hood (▶Fig. 3). The hood immediately became loose and was removed using a rat-tooth forceps (▶Fig. 4, ▶Video1). The submucosal tunnel was extended beyond the GEJ and the myotomy was completed. The patient made an uneventful recovery. This case illustrates that the hood can become dislodged in the submucosal tunnel during POEM and can usually be removed easily [1]. However, if it becomes difficult to remove the hood, as in the present case, myotomy should be carefully performed posteriorly to the hood, which should relieve the pressure in the tunnel and loosen the hood in the submucosal space. One should catch the hood from the mucosal side in order to avoid the prolapse of mucosa around the hood and to facilitate hood removal. Pulling the dislodged hood into the replacement hood will aid safe removal, as for the removal of a foreign body.


Annals of Hepatology | 2018

Comparison of Dynamic Changes Among Various Prognostic Scores in Viral Hepatitis-Related Acute Liver Failure

Shalimar; Ujjwal Sonika; Saurabh Kedia; Soumya Jagannath Mahapatra; Baibaswata Nayak; Dawesh P Yadav; Deepak Gunjan; Bhaskar Thakur; Harpreet Kaur; Subrat K. Acharya

INTRODUCTION AND AIM Multiple prognostic scores are available for acute liver failure (ALF). Our objective was to compare the dynamicity of model for end stage liver disease (MELD), MELD-sodium, acute liver failure early dynamic model (ALFED), chronic liver failure (CLIF)-consortium ACLF score and Kings College Hospital Criteria (KCH) for predicting outcome in ALF. MATERIALS AND METHODS All consecutive patients with ALF at a tertiary care centre in India were included. MELD, MELD-Na, ALFED, CLIF-C ACLF scores and KCH criteria were calculated at admission and day 3 of admission. Area under receiver operator characteristic curves (AUROC) were compared with DeLong method. The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), likelihood ratio (LR) and diagnostic accuracy (DA) were reported. RESULTS Of the 115 patients included in the study, 73 (63.5%) died. The discrimination of mortality with baseline values of prognostic scores (MELD, MELD-Na, ALFED, CLIF-C ACLF and KCH) was modest (AUROC: 0.65-0.77). The AUROC increased on day 3 for all scores, except KCH criteria. On day 3 of admission, ALFED score had the highest AUROC 0.95, followed by CLIF-C ACLF 0.88, MELD 0.81, MELD-Na 0.77 and KCH 0.52. The AUROC for ALFED was significantly higher than MELD, MELD-Na and KCH (P < 0.001 for all) and CLIF-C ACLF (P = 0.05). ALFED score ≥ 4 on day 3 had the best sensitivity (87.1%), specificity (89.5%), PPV (93.8%), NPV (79.1%), LR positive (8.3) and DA (87.9%) for predicting mortality. CONCLUSIONS Dynamic assessment of prognostic scores better predicts outcome. ALFED model performs better than MELD, MELD, MELD-Na, CLIF-C ACLF scores and KCH criteria for predicting outcome in viral hepatitis- related ALF.INTRODUCTION AND AIM Multiple prognostic scores are available for acute liver failure (ALF). Our objective was to compare the dynamicity of model for end stage liver disease (MELD), MELD-sodium, acute liver failure early dynamic model (ALFED), chronic liver failure (CLIF)-consortium ACLF score and Kings College Hospital Criteria (KCH) for predicting outcome in ALF. MATERIALS AND METHODS All consecutive patients with ALF at a tertiary care centre in India were included. MELD, MELD-Na, ALFED, CLIF-C ACLF scores and KCH criteria were calculated at admission and day 3 of admission. Area under receiver operator characteristic curves (AUROC) were compared with DeLong method. The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), likelihood ratio (LR) and diagnostic accuracy (DA) were reported. RESULTS Of the 115 patients included in the study, 73 (63.5%) died. The discrimination of mortality with baseline values of prognostic scores (MELD, MELD-Na, ALFED, CLIF-C ACLF and KCH) was modest (AUROC: 0.65-0.77). The AUROC increased on day 3 for all scores, except KCH criteria. On day 3 of admission, ALFED score had the highest AUROC 0.95, followed by CLIF-C ACLF 0.88, MELD 0.81, MELD-Na 0.77 and KCH 0.52. The AUROC for ALFED was significantly higher than MELD, MELD-Na and KCH (P < 0.001 for all) and CLIF-C ACLF (P = 0.05). ALFED score > 4 on day 3 had the best sensitivity (87.1%), specificity (89.5%), PPV (93.8%), NPV (79.1%), LR positive (8.3) and DA (87.9%) for predicting mortality. CONCLUSIONS Dynamic assessment of prognostic scores better predicts outcome. ALFED model performs better than MELD, MELD, MELD-Na, CLIF-C ACLF scores and KCH criteria for predicting outcome in viral hepatitis-related ALF.


Journal of clinical and experimental hepatology | 2017

Hepatocellular Carcinoma: An Unusual Complication of Longstanding Wilson Disease

Deepak Gunjan; Shalimar; Neeti Nadda; Saurabh Kedia; Baibaswata Nayak; Shashi Bala Paul; Shivanand Gamanagatti; Subrat K. Acharya

Wilson disease is caused by the accumulation of copper in the liver, brain or other organs, due to the mutation in ATP7B gene, which encodes protein that helps in excretion of copper in the bile canaliculus. Clinical presentation varies from asymptomatic elevation of transaminases to cirrhosis with decompensation. Hepatocellular carcinoma is a known complication of cirrhosis, but a rare occurrence in Wilson disease. We present a case of neurological Wilson disease, who later developed decompensated cirrhosis and hepatocellular carcinoma.


Digestive Diseases and Sciences | 2017

Acute Liver Failure Due to Hepatitis E Virus Infection Is Associated with Better Survival than Other Etiologies in Indian Patients

Shalimar; Saurabh Kedia; Deepak Gunjan; Ujjwal Sonika; Soumya Jagannath Mahapatra; Baibaswata Nayak; Harpreet Kaur; Subrat K. Acharya


Journal of clinical and experimental hepatology | 2018

Controlled Attenuation Parameter for Assessment of Hepatic Steatosis in Indian Patients

Gyanranjan Rout; Saurabh Kedia; Baibaswata Nayak; Rajni Yadav; Prasenjit Das; Subrat K. Acharya; Deepak Gunjan; Vishwajeet Singh; Mousumi Mahanta; Swatantra Gupta; Sandeep Aggarwal; Shalimar


Journal of clinical and experimental hepatology | 2018

Therapy with Oral Directly Acting Agents in Hepatitis C Infection Is Associated with Reduction in Fibrosis and Increase in Hepatic Steatosis on Transient Elastography

Gyanranjan Rout; Baibaswata Nayak; Arpan H. Patel; Deepak Gunjan; Vishwajeet Singh; Saurabh Kedia; Shalimar


Journal of clinical and experimental hepatology | 2018

13. Thromboelastography guided blood product transfusion in cirrhosis patients with acute variceal bleeding: a randomized controlled trial

Gyanranjan Rout; Deepak Gunjan; Saurabh Kedia; Baibaswata Nayak; Soumya Jagannath Mahapatra; A. Iqbal; Shalimar

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Baibaswata Nayak

All India Institute of Medical Sciences

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Saurabh Kedia

All India Institute of Medical Sciences

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Shalimar

All India Institute of Medical Sciences

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Subrat K. Acharya

All India Institute of Medical Sciences

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Gyanranjan Rout

All India Institute of Medical Sciences

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Ujjwal Sonika

All India Institute of Medical Sciences

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Harpreet Kaur

All India Institute of Medical Sciences

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Shekhar Jadaun

All India Institute of Medical Sciences

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Shivanand Gamanagatti

All India Institute of Medical Sciences

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Soumya Jagannath Mahapatra

All India Institute of Medical Sciences

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