Dose Steroid Therapy Research Articles

The clinical value of 4-hour delayed-enhanced 3D-FLAIR MR images in sudden hearing loss.

The aim of this study was to investigate the clinical significance of 4-hour delayed-enhanced 3.0 Tesla (3T) 3D-fluid-attenuated inversion recovery (FLAIR) MR imaging in sudden sensorineural hearing loss (SSNHL). Case series with comparisons. Tertiary referral centre. Eighty-seven idiopathic SSNHL patients were enrolled between January 2015 and December 2016 and received high dose steroid therapy and intratympanic steroid injections as salvage treatment. Pre-contrast, 10-minute and 4-hour delayed-enhanced 3D-FLAIR MR images were obtained using double-dose IV gadolinium. The results of treatment were evaluated according to Siegel's criteria 3months after the start of treatment. Where possible lesion-side laterality of the inner ear was identified based on the MR images, the associations between MR findings and other clinical parameters were analysed, and the relationships between hearing recovery and MR image findings were assessed. Lesion-side laterality was identified on MRI in 52 (59.7%), 18 (20.1%) and 8 (9.2%) patients, based on 4-hour delayed, 10-minute delayed, and pre-contrast images, respectively. The hearing recovery rate was significantly lower in the patients with lesion-side laterality on 4-hour delayed images (P<0.001). In a multivariate analysis, lesion-side laterality on 4-hour delayed images was associated with poor prognosis (OR=5.6) after adjusting other prognostic factors including initial hearing level, lesion-side laterality on 10-min delayed images and presence of vertigo. In addition, as the extent of enhancement in the inner ear increased the probability of hearing recover decreased (P=0.001). Contrast enhancement of inner ear structures can be seen on 4-hour delayed-enhanced 3T 3D-FLAIR MR images in idiopathic SSNHL. Asymmetric lesion-side enhancement of the inner ear may be associated with a poor prognosis.

Diagnostic Strategy and Therapeutic Dilemma in Acute Posterior and Panuveitis

Acute posterior and panuveitis mostly affect younger patients and affect both eyes in more than half of cases. Because of the severe consequences in the clinical course, rapid and broad differential diagnosis are critical steps. Permanent loss of vision after a delay in starting therapy and the initiation of ineffective treatment are both serious risks. The initial diagnostic classification is based on clinical presentation (anatomical localisation and type of inflammation) and clinical course and, secondarily, on the response to acute therapy. The aetiology is acute in as many as one third of cases. The most frequent acute posterior uveitis in immunocompetent persons is acute viral retinal necrosis. It is difficult to distinguish this clinically from Behçet uveitis, as long as there are no systemic manifestations. In patients with disease threatening the macula, high dose steroid therapy must be started no later than 24 hours after the start of antiviral and anti-parasitic acute therapy. Thus, misdiagnosis has therapeutic consequences. Moreover, the prognosis is favourably affected by aggressive treatment of acute posterior uveitis. Any delay in starting therapy increases infectious and inflammatory tissue damage, and increases the risk of involvement of the other eye and of other organs. On the other hand, the use of high doses of steroids, immunosuppressives and biological agents can lead to uncontrolled proliferation of the pathogen and relapses.

Analytical study of 100 cases of traumatic optic neuropathy

INTRODUCTION: Traumatic optic neuropathy is a devastating potential complication of closed head injury. The hallmark of an optic neuropathy, traumatic loss of visual function, which can manifest by subnormal visual acuity, visual field loss, or colour vision dysfunction. The presence of an afferent pupillary defect strongly suggests a prechiasmal location for the injury and is necessary to validate the diagnosis of traumatic optic neuropathy. Vision loss associated with traumatic optic neuropathy can be partial or complete and temporary or permanent. Approximately 1.5% to 5% of patients with closed head injuries have damage to visual pathways (4-6 / 100,000 general population / yr). These injuries can be divided into anterior and posterior lesions. Anterior lesions shows ophthalmoscopic abnormalities (eg. Central retinal artery occlusion) and usually associated with a variety of easily recognized injuries to the globe. Anterior lesions may include optic nerve avulsion, traumatic anterior ischemic optic neuropathy, anterior optic nerve sheath hematoma. Posterior lesions are free of ophthalmoscopic findings, but disc edema and disc pallor do occur. Posterior traumatic optic neuropathy is characterised by visual loss that occur in the presence of an afferent pupillary defect but without evidence of injury to the eye or optic nerve. AIM AND OBJECTIVES: To analyse the clinical profile, response to mega dose steroid therapy and visual function outcome in patients with traumatic optic neuropathy presenting to the neuroophthalmology clinic at Regional Institute of Ophthalmology and Government Ophthalmic Hospital, Chennai. MATERIALS AND METHODS: A prospective observational case study on the pattern of traumatic optic neuropathy and analysis of clinical profile, response to treatment and visual function outcome was conducted in the department of neuroophthalmology at RIO-GOH, Chennai. The study was conducted from June 2008 to November 2010. All eligible traumatic optic neuropathy patients according to inclusion criteria, presented to the neuroophthalmology clinic at RIO-GOH during June 2008 to may 2010 were included in the study. DISCUSSION Hippocrates might have been the first to identify the phenomenon of acute and delayed vision loss after injuries placed to and slightly above the brow. While there is little controversy on the macroscopic mechanism of trauma theory, multiple hypothesis have been proposed at microscopic level of damage to the optic nerve including contusion necrosis, nerve fibre tears and nerve infarction secondary to closed space edema, haemorrhage, thrombosis, vasospasm, impingement by bone spicules and shearing of dural vessels in the optic canal. In our study it is evident that traumatic optic neuropathy is devastating cause of permanent visual loss. Concussive force to head especially forehead transmits shock wave to optic canal. Visual loss is usually instantaneous. SUMMARY: Traumatic optic neuropathy is a rare but significant cause of post traumatic visual loss. The responsible blunt trauma to the frontal region may be minor or severe and accompanied by multiple adjacent fractures. Careful documentation of visual acuity, pupillary function, and red desaturation is essential to guide management. CT imaging should be performed to document such structural abnormalities as optic nerve avulsion, optic nerve sheath hematoma, orbital hematoma, or optic canal fracture with fragments. Based on the data from the International Optic Nerve Trauma Study, observation without intervention is a viable option. Patients and their families should be made aware of the information regarding mega dose corticosteroid therapy and participate in an informed decision. In particular, if visual acuity begins to deteriorate, then corticosteroid therapy should be considered. If a structural abnormality is present that may be contributing to optic nerve dysfunction (hematoma or fragment) or if the patient’s visual acuity deteriorates on corticosteroids, optic canal decompression should be offered. Management of this disorder remains very controversial; involvement of other appropriate subspecialists and careful discussions with the patient and family are essential to maximize visual outcome. FUTURE AND CONTROVERSIES: A better understanding of the cellular and biochemical mechanisms involving normal and traumatized axons, glia, and myelin sheaths may eventually leads to better intervention for traumatic optic neuropathy. Although corticosteroids are a type of neuroprotective agents, the recent expansion in basic scientific research regarding other neuroprotective agents may lead to a redirection in future therapy for this condition. CONCLUSION: In our study the clinical profile of 100 eligible patients who presented with loss of vision following trauma during June 2008 – May 2010 were analyzed. RESULTS: Based on exclusion and inclusion criteria 100 cases were taken up for the study.

When Gastroenteritis Is too Mainstream: Eosinophilic Gastroenteritis

Eosinophilic gastroenteritis (EGE) represents one member within the spectrum of diseases collectively referred to as eosinophilic gastrointestinal disorders (EGIDs), which includes eosinophilic esophagitis (EoE), gastritis (EG), duodenitis (ED), enteritis, and colitis. To our knowledge, this is the only case in literature with such as extensive involvement of the GI tract. A 46-year-old obese Caucasian male presented with three weeks of right upper quadrant (RUQ) pain, radiating to the back, which began in the mid-epigastric region, episodes of bilious vomiting, diarrhea, and fever. His labs showed white blood cells (WBC)- 16.1 K/uL (neutrophils- 50.6%, lymphocytes- 12.1%, eosinophils-34.3%). Computerized tomography (CT) abdomen and pelvis- ileitis. Esophagoduodenoscopy (EGD) showed gastritis and duodenitis. Mucosal biopsies showed duodenitis without eosinophilic infiltration. He was managed with intravenous antibiotics and IV methylprednisolone 20 mg Q 12 hourly. He was discharged on prednisone taper but was readmitted ten days later as the dose of prednisone came down to 10 mg QD. His Labs showed WBC- 14.7 K/uL (neutrophils-72.5%, lymphocytes-19.2%, eosinophils- 2.8%. CT abdomen and pelvis showed duodenitis and ileitis. An extensive workup done was inconclusive. He was discharged on a steroid taper. He was readmitted four months later due to acute on chronic, epigastric, non-radiating abdominal pain. His labs showed WBC- 20.3 K/uL (eosinophils- 38%), serum IgE- 134 kU/L. CT abdomen and pelvis showed esophagitis, duodenitis, enteritis, and colitis. EGD showed gastritis and duodenitis. Flow cytometry, JAK2, BCR-ABL to rule out eosinophilic malignancies were unremarkable. He was managed with steroid taper and discharged on chronic low dose steroid therapy. Six months after discharge, he is clinically stable on prednisone 2 mg per day. It is vital to differentiate EGE from secondary diseases associated with eosinophilia of an identifiable cause. This entity emphasizes the importance of an invasive approach along with a thorough medical history; findings on physical examination are not useful for reaching the diagnosis, hence being fundamentally histological. Corticosteroid therapy in EGE is an imperfect compromise between a dose that yields a tolerable level of systemic side effects and only partial treatment of symptoms. There are no clinical guidelines available for EGE, and it remains underdiagnosed, with an uncertain prognosis.2588 Figure 1. Mucosal Biopsy Showing Gastritis And Duodenitis

A Retrospective Case Series of Granulomatosis with Polyangiitis Complicated by Bowel Perforation After High Dose Steroid Therapy

A Retrospective Case Series of Granulomatosis with Polyangiitis Complicated by Bowel Perforation After High Dose Steroid Therapy

Granulocyte-Colony Stimulating Factor 투여 후 발생한 돌발성 난청

Filgrastim® (Granulocyte-colony stimulating factor, G-CSF) is generally used to promote the increase of neutrophils to patients with neutropenia during chemotherapy or donors for hematopoietic stem cell transplantation (HSCT). Its adverse effects were mainly reported as non-serious symptoms, such as back pain, headache, arthralgia and fever. A 29-year-old male was administered the Filgrastim as a HSCT donor. He accompanied left side hearing disturbance and tinnitus after 2 days from administration of the drug. He admitted to our department and underwent improvement of hearing after high dose steroid therapy. In this report, we describe a case of sudden sensorineural hearing loss (SSNHL) as an unreported adverse effect of G-CSF in the literature. (J Clinical Otolaryngol 2018;29:87-90)

Pediatric Relapsing Anti-NMDAR Encephalitis Crossing with Tumefactive Demyelinating Lesion

AbstractAnti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune encephalopathy characterized by neuropsychiatric symptoms, autonomic instability, and abnormal movements. Most children who undergo tumor removal and receive appropriate immunosuppressants have substantial neurological improvement. We report a 14-year-old girl with relapsing anti-NMDAR encephalitis who presented with paroxysmal tingling and weakness of the right lower limb. Despite long-term prophylaxis with immunotherapy (azathioprine), tumefactive demyelinating lesion and multifocal subcortical white matter lesions were identified on magnetic resonance imaging, which improved after high doses of steroid therapy. There may be overlap between the clinical manifestations of anti-NMDAR encephalitis and acquired demyelination syndromes in children.

Self-limiting Ibrutinib-Induced Neutrophilic Panniculitis

Neutrophilic panniculitis is a relatively rare condition, characterized by predominantly neutrophilic inflammation in the subcutaneous fat. Rarely, neutrophilic panniculitis may be induced by chemotherapeutics or targeted molecular therapies, including the Bruton tyrosine kinase inhibitor ibrutinib. Previously reported cases of ibrutinib-induced panniculitis were suppressed with sustained low-dose steroid therapy while continuing ibrutinib therapy. To our knowledge, self-limiting panniculitis during ibrutinib therapy has not yet been described. We describe a case of self-limiting, neutrophilic panniculitis which developed during ibrutinib therapy. A 78-year-old woman presented to the dermatology clinic with a 3-week history of painful erythematous nodules on her lower extremities which occurred 1 month after initiating ibrutinib therapy for chronic lymphocytic leukemia. Physical examination revealed tender erythematous poorly demarcated subcutaneous nodules on the anterior and posterior aspects of both lower legs. A panniculitis was suspected clinically, and a punch biopsy was performed. Histological evaluation revealed a lobular panniculitis with fat necrosis and infiltrates consisting predominantly of neutrophils. A diagnosis of neutrophilic panniculitis was rendered, which the patient opted not to treat. The eruption waned before resolving spontaneously over the course of 6 months despite continued ibrutinib therapy. This case illustrates panniculitis as an emerging adverse drug reaction after treatment with ibrutinib and that not all cases will require ibrutinib dose adjustment or steroid therapy but rather may be subject to spontaneous resolution.

Extranodal Rosai-Dorfman disease involving paranasal sinuses, orbits and anterior cranial fossa

Rosai-Dorfman disease (RDD) is a rare, benign pseudolymphatous condition, predominantly involving lymph nodes. Although several cases of extra-nodal involvement have been reported previously, central nervous system involvement, particularly in the absence of nodal disease is extremely rare. Extranodal large RDD presenting as a single lesion involving sino-orbital and anterior cranial fossa has rarely been described previously. We report a case of incisional biopsy proved RDD in a young lady who presented with nasal obstruction and subsequent proptosis with visual diminution. Radiography of head and paranasal sinus demonstrated a strongly enhanced, diffuse polypoid lesion filling the bilateral sinonasal cavity and orbit with extension to the anterior cranial fossa by way of splaying the bony foramina. Pre-operative low dose steroid therapy had resulted in decreased size of the mass which facilitate gross-total surgical resection. RDD was confirmed by histopathology (emperipolesis) and immuno-histochemistry (S-100 positivity). The follow-up computed tomography 3 months later showed minimal tumor residue in left parasellar region with complete sinonasal decompression.

Urinary neutrophil gelatinase-associated lipocalin as prognostic biomarker for idiopathic nephrotic syndrome in Egyptian children

Background and Objectives: It is important to distinguish steroid sensitive nephrotic syndrome (SSNS) from steroid resistant nephrotic syndrome (SRNS) to avoid initial full dose steroid therapy in the latter. Neutrophil gelatinase-associated lipocalin (NGAL) is a biomarker of acute kidney injury (AKI) even on top of chronic kidney disease (CKD). The aim is to determine urinary NGAL level in children with idiopathic nephrotic syndrome (INS) as a prognostic factor for INS, it can predict steroid resistance early in the course of INS. Subjects and Methods: The present study was carried out on ninety children with INS who were admitted in Pediatric Nephrology Unit of Tanta University Hospital. Thirty healthy children of the same age and sex served as control group. The subjects were subdivided into three groups: Group 1 (SSNS), Group 2 (SRNS), and Group 3 (controls). Patients and controls were subjected to clinical evaluation, laboratory investigations which included 24 h urinary collection for urinary volume and protein, complete blood count, serum cholesterol, serum albumin, blood urea, serum creatinine, and urinary NGAL measurement by enzyme-linked immunosorbent assay. Results: There was a significant increase in uNGAL levels in SRNS when compared with SSNS or controls. There was no significant difference in uNGAL levels between Group 1 and Group 3. ROC curve of uNGAL to predict SRNS had cutoff value >315 at the area under the curve 0.9, sensitivity 86.7%, and specificity 93.3%. There was a significant positive correlation between urinary NGAL level and age of patients and disease duration and serum creatinine level. Conclusions: Urinary NGAL can predict SRNS in INS in children.

Standard Versus Low Dose Steroid Therapy in the First Attack of Childhood Nephrotic Syndrome

The Nephrotic syndrome is one of the commonest renal diseases in children .The word ‘Nephrosis”or what is often called primary nephritic syndrome had its origin in the early part of 20 th century and was described as a clinical condition of edema and proteinuria where the Kidney demonstrated (light microscopy) degeneration of tubule associated with renal glomeruli. The problem of Nephrotic syndrome continues to pose a major challenge in paediatric nephrology.Although the disease may affect 2 children per 1,00,000 annually ,most patients suffer from a chronic course that last several years.There is considerable associated morbidity and a significant proportion of patient may eventually develop end stage renal disease. Even in the mildest from of nephrotic syndrome i.e the child withMCNS is manifested by an intial attack 1. May require hospitalization, 2. A prolonged period of initial treatment ( i.e a minimum of 8weeks) 3. Require frequent monitoring both at home and by physician visits, 4. Require a treatment program with a drug having known and significant adverse effects 5. Has a high rate of recurrence i.e relapse in >60% cases 6. Where relapse are having associated with common illness acquired every day activities i.e day care,school,and gatheringand additionally where the progression of chronic renal failure is always there.

Tuberculosis Meningitis with Brainstem Mass Lesion—Adjunctive Treatment with Thalidomide: A Case Report

Background: We report on a 12-month-old child with recurrence of intracranial tuberculosis after de-escalation of the initial therapy with levofloxacin, rifampicin, ethambutol, and pyrazinamide in an outpatient clinic. After initial improvement of atactic movement disorder with ongoing motoric and mental development the child deteriorated with progressive impairment of vigilance. Magnetic resonance imaging (MRI) of the brain showed meningitis together with a cerebellar abscess and brainstem mass lesion resulting in increased intracranial pressure. Surgical decompression was incomplete due to massive granuloma formation in the basal meninges. Postinterventional the child remained comatose and showed extension spasm. Besides reinitiation of the tuberculostatic therapy (adjusted after blood and CSF concentrations) with rifampicin, pyrazinamide, prothionamide and levofloxacin we started high dose steroid therapy to reduce intracranial edema. Tuberculosis abscess and mass lesions tend to induce an inadequate tumor necrosis factor (TNF)-α–dependent cytokine response. Therefore additional treatment with the TNF-α inhibitor thalidomide was started to control the intracranial tuberculosis granuloma formation and to reduce steroid therapy. After five months of treatment the MRI showed regression of the tuberculous mass lesion and the patient caught up on motoric and mental development.

Lack of Association between Pulse Steroid Therapy and Bone Mineral Density in Patients with Multiple Sclerosis.

Multiple sclerosis (MS) has been associated with reduced bone mineral density (BMD). The purpose of this study was to determine the possible factors affecting BMD in patients with MS. We included consecutive 155 patients with MS and 90 age- and sex-matched control subjects. Patients with MS exhibited significantly lower T-scores and Z-scores in the femoral neck and trochanter compared to the controls. Ninety-four (61%) patients had reduced bone mass in either the lumbar spine or the femoral neck; of these, 64 (41.3%) had osteopenia and 30 (19.4%) had osteoporosis. The main factors affecting BMD were disability, duration of MS, and smoking. There was a negative relationship between femoral BMD and EDSS and disease duration. No association with lumbar BMD was determined. There were no correlations between BMD at any anatomic region and cumulative corticosteroid dose. BMD is significantly lower in patients with MS than in healthy controls. Reduced BMD in MS is mainly associated with disability and duration of the disease. Short courses of high dose steroid therapy did not result in an obvious negative impact on BMD in the lumbar spine and femoral neck in patients with MS.

Acute Respiratory Failure due to Neuromyelitis Optica Treated Successfully with Plasmapheresis.

Neuromyelitis Optica (NMO) is a demyelinating autoimmune disease involving the central nervous system. Acute respiratory failure from cervical myelitis due to NMO is known to occur but is uncommon in monophasic disease and is treated with high dose steroids. We report a case of a patient with NMO who developed acute respiratory failure related to cervical spinal cord involvement, refractory to pulse dose steroid therapy, which resolved with plasmapheresis.

Syndrome of Remitting Seronegative Symmetrical Synovitis with Pitting Edema (RS3PE): A Case Report and Review of the Literature

Remitting Seronegative Symmetrical Synovitiswith Pitting Edema (RS3PE) is a rare clinical entitythat is easilymissed due to lack of knowledge. Syndrome is characterized by suddenonset of edema with swellingon thedorsum of thehandsand by synovitis. Serological tests are negative and radiographic joint destruction does not occurs. Etiology of RS3PE syndrome is not known. It can occur as an idiopathic phenomenon, but also is in association with rheumatic diseases. In addition, several reports have described RS3PE as a paraneoplasticsyndrome can occuron concomitantly with both hematological and solidmalignancies. Because of this clinical association, it is not very easy to diagnose this syndrome. We discuss a case of RS3PE where the patient presented with acute onset polyarthritis and pitting edema of the extremities without an underlying systemic cause. Patient showed dramatic response with low dose steroid therapy.

Acute Diseminated Encephalomyelitis: A Case Report and Review of Literature / Akut Disemine Ensefalomiyelit; Olgu Sunumu Ve Literatur Incelemesi

Acute disseminated encephalomyelitis (ADEM) is an autoimmune and monophasic central nervous system disease that principally affects brain and spinal cord by causing non-vasculitic inflammatory diffuse demyelination. ADEM is one of the rare causes of impaired consciousness in childhood. Incidence of the disease under the age of 20 is 1.5-3 / 100000 per year and it mostly occurs in children between the ages of 5-8 years. Underlying causes aren't defined clearly yet, however, infections and vaccinations are known as predisposing factors for the disease. Multifocal white matter lesions on magnetic resonance imaging (MRI) are characteristic signs of ADEM. In our case, hyperintense lesions in cerebrum were detected on cranial MRI subsequent to impaired consciousness and convulsion. No specific feature was found in cerebrospinal fluid analysis of the patient. In this paper, we present a three-year-old boy who developed ADEM subsequent to viral upper respiratory tract infection and had full recovery after high dose steroid therapy.

Massive Serositis as the Initial Presentation of Systemic Lupus Erythe-matosus: A Report of Two Cases and Review of the Literature

Large volume effusions as a manifestation of active systemic lupus erythematous (SLE) is rare, and when it does occur, it is usually associated with complications of chronic lupus disease, such as nephrotic syndrome, constrictive pericarditis, heart failure or Budd-Chiari syndrome. Massive serositis as a presenting feature of SLE is rare. We de-scribe two adult cases of new onset SLE presenting with massive ascites in the first case, and large bilateral pleural effusions in the second case. The serositis in both patients responded well to high dose steroid therapy with signifi-cant improvement in symptoms. Only a small number of case reports describing massive ascites or large pleural effusions as initial manifestations of new onset SLE have been published. A literature review of these case reports and their treatment outcomes is described.

The clinical phenotype of Israeli patients with Q703K mutation in the NLRP3 gene

Results Seven female and 3 male patients with a mean age of 22.5±17.8 years and a mean diagnosis delay of 12.4 years were identified. Their clinical characteristics ranged from self resolving attacks of fever, urticaria and arthralgia to a chronic, debilitating steroid-dependent inflammatory disease. Splenomegaly, transfusion-dependent anemia, sensory neuropathy and pericarditis, manifestations which are not included in the traditional CAPS-spectrum, were detected in some of the patients. The majority of patients responded to high dose steroid therapy. DMARDS such as methotrexate, azathioprine and colchicine were generally ineffective at reducing steroid dose or attack rate. Therapy with TNF inhibitors or anti IL-1 agents was instituted in 4 patients with a favorable response. All but one patient needed chronic anti-inflammatory therapy to prevent attacks and reduce steroid dose.

Guidelines for treatment of septic shock in resource limited environments

WHO 2005 data points to sepsis in form of pneumonia, diarrhea, and neonatal sepsis as major killers of children in the resource limited countries of Asia and Africa, However, currently there are no specific published guidelines for treatment of severe sepsis in resource limited circumstances. An expert panel drawn from all over India, met to discuss and draw guidelines for management of pediatric septic shock that are applicable to resource limited countries. The group evaluated strength of published data and expert opinion for clinical practice and feasibility of delivery of care at various levels of resource constraints, keeping in view unique patient population and limited availability of equipment and resources. Issues for discussion included simplified definitions and reliable clinical indicators of septic shock, fluid resuscitation, graded inotropic and vasopressor support, corticosteroid therapy, timing and indication for endotracheal intubation and use of positive end expiratory pressure/mechanical ventilation, initial empirical antibiotic therapy, correction of hypoglycemia and glycemic control, role of immunoglobulin, and blood and blood products. Evidence has been graded and levels of evidence indicated wherever applicable. The expert group recognized and listed potential barrier to implementation of existing American College of Critical Care Medicine guidelines for treatment of septic shock in resource limited countries, adopted simplified definitions of septic shock, tachycardia, tachypnea and hypotension, and developed step-wise algorithmic approach for treating septic shock. Evidence based treatment recommendations include early oxygen therapy, fluid resuscitation based on blood pressure, use of dopamine in fluid refractory shock, early use of antibiotics, early intubation and assisted ventilation, correction of hypoglycemia and emphasis on use of physical examination for achieving therapeutic endpoints. These interventions have brought the mortality down and can be easily applied even at primary and/or secondary level health facilities. Interventions recommended after above steps were based on consensus rather than evidence. These include stress dose steroid therapy, use of vasopressors and inodilators, and central venous pressure and echocardiography to guide fluid and vasoactive drug infusion, which require transfer to a pediatric intensive care unit. Strict glycemic control is not recommended. Evidence on benefit of several other interventions viz. use of vasopressin as vasopressor, use of intravenous immunoglobulins, renal replacement therapy, use of plasmapheresis etc. is emerging. The expert group observed that further research evaluating individual components of guidelines and relative benefit of each of these interventions in resource limited setting is needed, as also the benefit of adherence with standardized protocol. Pediatric sepsis guidelines suitable for resource limited settings are presented for resource limited settings. Several unresolved issues were identified for further research.

Acute Amiodarone Pulmonary Toxicity after Drug Holiday: A Case Report and Review of the Literature.

Amiodarone is reported to cause a wide continuum of serious clinical effects. It is often challenging to detect Amiodarone-induced pulmonary toxicity (AIPT). Typically, the diagnosis is made based on the clinical settings and may be supported by histopathology results, if available. We describe a 57-year-old patient who developed severe rapidly progressive respiratory failure secondary to AIPT with acute bilateral infiltrates and nodular opacities on chest imaging. Interestingly, Amiodarone was discontinued 3 weeks prior to his presentation. He had normal cardiac filling pressures confirmed by echocardiography. To our knowledge, this is the first case of isolated acute lung injury induced by Amiodarone, three weeks after therapy cessation, with adequate clinical improvement after supportive management and high dose steroid therapy.