Emergency department involves challenging care for undifferentiated and unexpected patients with critical illnesses or injuries requiring immediate medical attention. It has a vital role in triaging the patients and making the proper diagnosis for their better management.

Aim and objectives:

The aim of this study is to evaluate diagnostic accuracy in the Emergency Department and the role of clinical diagnosis and impact of addition of point of care testing and imaging in the process of making a diagnosis in a tertiary care teaching hospital in northeast India.

Materials and methods:

Retrospective cohort study in a single tertiary level teaching Superspeciality hospital in Northeast India where approximately 600 patients gets admitted through ED every month. It is purely an observational study and no intervention was done.

The provisional diagnosis at the time of presenting to ED andthe final diagnosison discharge were compared and were analyzed statistically. Diagnosis are made based on presenting complaints, past medical/surgical history, physical examination, point of care tests and radiological imaging. The patient were categorized into three groups/catagories:

Category A:  History +Physical examination alone.

Category B:  Cat A + Point of care Tests

Category C:   Cat B + Radiological imaging

Results:

A total of 200 patients were there in the sample size.

Discussion:

There are very few studies on correlation between emergency department diagnosis and final diagnosis till today. Thus, the present study may be used as a baseline for future study, clinical audit or other quality assurance in the field of diagnostic accuracy in emergency department.

The duration of this study is period of one month among 200 admitted patients from ED. A total of 157 patients (78.5%)were diagnosed accuratelywhilein 43 patients (21.5%) the diagnosis wasincorrect.The maximum correct diagnosiswere seen in Cat C group (85.13%) and maximum incorrect diagnosis were seen in Cat A group. And from the calculation it was clear that with the use of point of care testing the diagnostic accuracy is increasing which was further increased by the use of imaging. And in incorrect group the diagnostic inaccuracy was decreased by use of point of care testing which was further decreased by using imaging.

Conclusion:

ED is a dynamic environment where patients land up with various presenting complaints. At times it becomes difficult for ER physicians to evaluate a patient correctly due to time constraints. The ER physicians should take a brief concised and focused history with examination following to the pertaining ailment. Many newer POCTs (Point of Care Tests) have come in the recent time which helps to consolidate the admitting diagnosis with evidence. Of course working in ED one has to master the skill and art in performing history taking and physical examination in an efficient manner, which is the most important and rewarding diagnostic tools in ED which will help to achieve the higher accuracy rate.

• No conflict of interest is there by anyone in this study.
• No financial help taken from anyone.
• Ethical clearance was done.

Reference:

1. 2013 by the Society for Academic Emergency Medicine. US
2. 2016 by the Society for Academic Emergency Medicine.
3. Hongkong journal of emergency medicine a comparison of emergency department admission diagnosis and discharge diagnosis: retrospective study,2003.

Author:

1. Dr. Yaseng Pegu, Fellow, Emergency Medicine (Narayana Superspeciality Hospital, Guwahati)
2. Dr. Apurba Kumar Borah, HOD, Critical Care and Emergency Medicine (Narayana Superspeciality Hospital, Guwahati)
3. Dr. Soumar Dutta, Consultant and Coordinator, Emergency Medicine (Narayana Superspeciality Hospital, Guwahati)

The post Evaluation of Diagnostic Accuracy in Emergency Department and role of clinical, point of care testing and imaging in it in a tertiary care teaching hospital in northeast India. appeared first on CCEM Journal.

Urea cycle is the  final pathway for nitrogen metabolism. Urea cycle disorders are inherited deficiencies of the enzymes involved in the cellular excretion of excess ammonia produced during protein metabolism. Although the majority of recognized patients are children, a delayed presentation is seen in patients with partial enzyme deficiency, including heterozygotes. The diagnosis onlybecomes apparent during times of increasedmetabolic stress, such as with acute or chronic illness.The primary manifestations of elevated blood ammonium affect central nervous system.

Case Report :

A 42 years old gentleman, previously well, presented with history of right facial weakness for 7 days for which he was taking Tab Wysolone 60 mg/day, followed by malaise for 2 days with sleep disturbances and altered sensorium  for 1day. At presentation,he was irritable in a stuporous state. Initial possibilities considered ? Viral encephalitis.  He was   intubated and connected to ventilator. Initial routine investigations  were normal. He was started on acyclovir , Ceftriaxone and  antiepileptics.  MRI brain showed small T2/FLAIR subcortical hyperintensities. Next day he developed generalized tonic clonic seizures for which antiepileptics were further added.  However, seizures persisted and became violent in nature. In view of status epilepticus, he was started on Thiopentone infusion which controlled seizures. CSF study routine was normal.He was evaluated for other causes of encephalopathy and Serum ammonia was found to be high (1200μmol/L).Decided for dialysis and SLED was done. Ammonia detoxification were started.  In view of persisting comatose state ,CT brain was done which showed diffuse cerebral edema which was managed conservatively. He became haemodynamicallyunstable, requiring ionotropic support. Urea cycle disorder panel was sent. The patient expired on 7^th day since admission.

Discussion:

Most likely cause for hyperammonemia of our patient was thought to be urea cycle defect, ornithine transcarbamylasedefect  aggravated by steroid exposure for Bell’s paralysis. Reports followed,Urinary orotic acid was detected and urea cycle disorder panel showed Citrullininemia.

N-acetylglutamate is required for the urea  cycle to take place. Glutamic acid is first combined with Acetyl CoA by Nacetylglutamatesynthetase (NAGS) to create N-acetylglutamate. N-acetylglutamateactivates  carbamoyl phosphate synthetase I.

Ammonia is then coverted to carbamoyl phosphateby carbamoyl phosphate synthetase I (CPS I)   Ornithine transcarbamylase (OTC) then catalyzes a reaction between carbamoyl phosphate and ornithine to generate citrulline in the urea cycle. Finally urea is formed and  excreted. Deficiency in any five of the enzymes in the urea cycle results in theaccumulation of ammonia which could be potentially fatal if untreated.The most common deficiencies are Nacetylglutamatesynthetase (NAGS) deficiency, carbamoyl phosphate synthetase I (CPS I) deficiency, and ornithine transcarbamylase (OTC) deficiency. OTC and CPS deficiency patients may display a`low citrulline and arginine level in the metabolic panel. Urine studies in an OTC patient typically show a high level of orotic acid, which is a by-product of the cycle and is made from carbamoyl phosphate when OTC is not available. OTC is an X-linked disorder and can have a late presentation from carrier states in which there are varying amounts of residual enzyme activity.

Conclusion:

Although urea cycle defect is very rare in adult , there should be a strong suspicion and consider in patient with unexplained altered sensorium because delay in initiating treatment may cause devastating outcome.

Reference :

1. A Case of Suspected Urea Cycle Dysfunction in a Patient with Unexplained Hyperammonemia Christopher Perrone, Monica Makhija, and Ann Mitchell Department of Neurology University of Massachusetts Medical School, Worcester, MA
2. Smith W, Kishnani PS, Lee B, et al. Urea cycle disorders: clinical presentation outside the  newborn period. Crit Care Clin 2005;21:S9-17, http://dx.doi.org/10.1016/j.ccc.2005.05.007
3. Gardeitchik T, Humphrey M, Nation J, Boneh A. Early clinical manifestations and eating patterns in patients with urea cycle disorders. J Pediatr2012;161:328-332, http://dx.doi.org/10.1016/j.jpeds.2012.02.006
4. Atiq M, Holt AF, Safdar K, et al. Adult onset urea cycle disorder in a patient with presumed hepatic encephalopathy. J ClinGastroenterol2008;42:213-214, http://dx.doi.org/10.1097/01.mcg.0000225628.84168.25
5. Clay AS and Hainline BE. Hyperammonemia in the ICU. Chest 2007;132:1368-1378, http://dx.doi.org/10.1378/chest.06-2940
6. Lien J, Nyhan WL, Barshop BA. Fatal initial adult-onset presentation of urea cycle defect. Arch  Neurol2007;64:1777-1779, http://dx.doi.org/10.1001/)

Author:

1. Dr. RajibDuarah, Associated Consultant, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati)
2. Dr. Kundan Hazarika, Consultant, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati)
3. Dr. Apurba Kumar Borah, HOD, Critical Care and Emergency Medicine (Narayana Superspeciality Hospital, Guwahati)

The post Hyperammonemic encephalopathy due to urea cycle disorder: A Case Report appeared first on CCEM Journal.

Invassive fungal infection is a common problem faced in ICU’s of all over the world.If we went back to history, It started in 1835 by the discovery of a mould , beauvariabassiana by Agostino Bassi. Then Gruby discovered candidiasis (1842) and Sluyter discovered aspergillosis in 1847^1,2. The candida albicans was the most predominant yeast in ICUs, which is recently changing to non albicans³.

Aims and Objectives:

Aim of this study is to find out the commonest fungus in northeast part of India and their sensitivity pattern. This will help in decision making while treating invasive fungal infection in this part of the country.

Materials and Methods:

All the positive cultures of respiratory and urine samples were taken. The duration is from june’2017 till october’2017. A total of 28 positive samples were taken. We will continue to collect data’s and will come up with larger no in future.

Results:

Discussion and conclusion:

The commonest fungus found in our study is Candida Albicans (64.28%), followed by Candida Tropicalis, Candida Glabrata and Aspergillus Fumigatus – all in same position with 10.71%. There is 1 case of Candida Krusei which is resistant to fluconazole. Sensitivity pattern of aspergillus is under process and we will come up later. Interesting finding is about aspergillus which is getting more frequent.

We are continuing the study and trying to make it multicentre. We will come up with larger pull of data in future.

References:

1. Kisch B. Forgotten leaders in modern medicine: Valentin, Gruby, Remark, Auerback. Trans Am PhilosSoc1954;44:139-317.
2. Ajello L. Systemic mycoses in modern medicine. ContrMicrobiolImmunol1977;3:2-6
3. https://www.ncbi.nlm.nih.gov/pubmed/27837497

Author:

1. Dr.Apurba Kumar Borah, HOD, Critical care and Emergency Medicine (Narayana Superspeciality Hospital, Guwahati)
2. Dr. Vicky lahkar, Consultant Microbiologist (Narayana Superspeciality Hospital, Guwahati)
3. Dr.Avisekh Aggarwal, Consultant Pulmonologist (Narayana Superspeciality Hospital, Guwahati)
4. Dr.Kundan Hazarika, Consultant, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati)
5. Dr.Soumar Dutta, Consultant and Coordinator, Emergency Medicine (Narayana Superspeciality Hospital, Guwahati)

The post Epidemiology of Fungal infection in a tertiary care hospital in northeast India: A Retrospective study appeared first on CCEM Journal.

Intensive care unit is a highly dynamic area of a hospital with the sickest patient being managed very intensively. But beacause of super severity of illness the mortality rate is also significantly high. There are paucity of data in India in this regards.

Aim and Objective:

Aim Of the study is to find out the common disease processes involving in mortality so that more focus can be put in this areas.

Material and Method:

We have collected data from december’2016 to november’2017. The data collected from master register and final cause of death is noted from death certificate issued.

Results:

Discussion:

In our study we find that with 42.66% sepsis is the leading cause of death. Cardiac failure with 26.66% is in second position followed by Road traffic accidents(RTA) in 3^rd position with 9.77%. Fourth position is cerebrovascular accidents with 7.55%. 5^th position is chronic liver disease (CLD) with 4.88%. Renal failure is in 6^th position (4%), COPD is in 7^th position (1.77%), poisoning is in 8^th position (1.33%), post op is in 9^th position (0.88%) and Malignancy is in 10^th position (0.44%).

Conclusion:

Sepsis is the leading cause of death in ICU followed by Cardiac Failure and Road traffic Accidents.

Author:

1. Dr.Apurba Kumar Borah, HOD, Critical Care and Emergency medicine (Narayana Superspeciality Hospital, Guwahati, Assam)
2. Dr.ManashRanjanChaudhury, Fellow, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati, Assam)
3. Dr.Soumardutta, Consultant and Coordinator, Emergency Medicine (Narayana Superspeciality Hospital, Guwahati, Assam)
4. Dr.Sidhartha das, Associate consultant, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati, Assam)
5. Dr.Suman Nandi, Associate consultant, Critical care Medicine (Narayana Superspeciality Hospital, Guwahati, Assam)
6. Dr.Kundan Hazarika, Consultant, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati, Assam)

The post Evaluation of ICU mortality in a tertiary care hospital in northeast India appeared first on CCEM Journal.

Paraquat(chemically a dipyridyl compound) isa herbicide.It acts by producing local and systemic toxicity.Plasma and urine paraquat levels are strongly associated with mortality in acute poisoning. The usual mode of mortality in acute setting is multiorgan dysfunction while in sub-acute stage, lung fibrosis is the cause.The standard principles of resuscitation like assessment and management of airway,breathing and circulation should generally be followed as per routine guidelines. Mucosal toxicity or the presence of vomitus can severely compromise the airway. Metabolic acidosis, aspiration and/or acute alveolitis can produce respiratory failure. Oxygen should be used cautiously as the worse oxidative stress greatly increases lethality in animal models.

Case report:

A 25-year-old male patient with no significant medical history presented to ER with alleged history of consumption of paraquat. He was in a semi-conscious state with a BP of 128/70mm Hg, Pulse 90/min, RR 18/min and maintaining spo2 100% on room air.In the ER,IVFluid NS @ 100ml started after securing peripheral line with 18 G canula, gastric lavage with NS done. Activated Charcoal 50 Grams stat given. Inj. N. Acetylcystine (NAC) 8g IV stat given. Patient was shifted to ICU for further management.Initial Investigation showed Hb 14.7,WBC 14.5INR 1.23,S. Sodium 136,S. Potassium 4.17, S. creatinine 1.08ABG: pH 7.451, Pco₂ 35.2, Po₂ 120.2, HCO₃ 24.5. Charcoal hemoperfusion was started within 9 hours from ingestion.Patient was also started on N-Acetylcysteine infusion,Vitamin C,Vitamin E,Thiamine, Steroid and other supportive medications. Patient developed acute renal failure which was treated conservatively.Patient complained of pain on swallowing. He was kept nil per orally.Endoscopy was done which revealed erosive esophagitis.PEG was planned but thepain on swallowing decreasedsignificantly. So liquid diet was startedon day 4 of admission. Patient condition improved significantly and was shifted to ward on day 5.

Discussion:

Hsu etal. studied the role of early hemoperfusion (<4hrs)on survival in severe Paraquatpoisoning.They found that early hemoperfusion<4hrsor<5hrs was associated with a 62% and 41% reduction of relative risk of mortality of all severely poisoned patients,respectively. In our case we started the patient on charcoal haemofiltration after 9 hrs (approx.) of ingestion. The duration of haemofiltration was for 4 hours and done only once, which was well tolerated by the patient.Hypotension in these type of case usually responds to boluses of fluids. Renal failure usually developes during the first 24 hrs period so maintainance of volume status is very much crucial. Consciousness generally maintains in a normal level.Any impairment should prompt either co-ingestion of other agents(e.g.ethanol) or severe toxicity causing hypoxia,hypotension and severe acidosis.. This was the first patient survived in our centre with paraquat poisoning. Inspired by the result, we decide to publish the case. A written consent was taken before publishing.

Conclusion:

Consumption of significant amount of paraquat leads to extremely high mortality. Interestingly in our case we found charcoal haemofiltration along with anti oxidants can save some valuable lives, so we recommend strongly for early haemofiltration of such patients.

References:

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243009/#
2. https://reference.medscape.com/medline/abstract/28704509

Author:

1. Dr Sidhartha Das, Associate Consultant
2. Dr Soumar Dutta, Consultant Coordinator
3. Dr Apurba Kumar Borah Consultant and HOD,Department of Critical Care Medicine
4. Dr.Manash Choudhury, Fellow, FCCCM
5. Dr.Kundan Hazarika, Consultant, Critical Care Medicine
6. Dr.DipankarHaloi, Fellow, IDCCM

The post Saving Paraquat Poisoning A Casereport appeared first on CCEM Journal.

A common medical emergency is poisoning, irrespective of whether it is intentional or accidental. Poisoning is a significant global public health problem. According to WHO data, in 2012 an estimated 193,460 people died worldwide from accidental poisoning and a million people die every year because of self-poisoning with suicidal intent.

Introduction:

Sixty patients were enrolled in the study.This study describes 4 years profile of poisoning patients from September 2014 to October 2017 at a tertiary Care teaching hospital.The present study has been undertaken to identify/study as to what is the most common substance used as poison,the trends among different genders/age,the time interval between poisoning and arrival in Emergency department,the morbidity associated,mortality and some other aspects which we are going to discuss later on.

Context:

Poisoning is an acute medical emergency and is associated with a very high morbidity and mortality.Previously, the poisoning deaths from pesticides were mainly accidental but easy availability, low cost and unrestricted sale have led to an increase in suicidal and homicidal cases as well.  In the developed world, poisoning due to narcotics and drug over dosage is far more common than due to pesticides.

Aims:

Retrospective descriptive study to explore the epidemiological characteristics and clinical profile of patients presenting with poisoning in emergency department of a tertiary care teaching hospital in northeast India. ICU/Hospital length of stay,any mortality during stay and follow up after 28 days from 2014 to 2017 were done.

Population:

All the patients (irrespective of age) presented with the alleged history of any poisoning between the year 2014 to 2017 were screened from the emergency register. The patients who received the discharge diagnosis of “Alleged Poisoning” and confirmed poisoning were enrolled in the study. Confirmed poisoning cases were made out by clinical as well as laboratory testing. Autopsy reports of deceased patients of alleged poisoning cases were not available but nonetheless those cases were included in study.

Material and Method:

Institutional review board/ Ethics committee clearance with wavier of consent: Since this was a retrospective study and did not involve the disclosure of any individual patient identity, the consent was waived. All the patients (irrespective of age) presented with the alleged history of any poisoning between the year 2014 to 2017 were screened from the emergency register.

Results:

• Gender–  The males marginally outnumbered female patients. Though majority of the patients were males, profession wise females showed uniformity in being Housewives while male patients had varied background from students to farmers to workers.
• Cause– Poisoning with suicidal intent was more frequent (>90%) than accidental.
• Time Interval– The mean time interval between poison consumption and arrival to hospital was 4.7 hours.
• Characteristics-The most common type of substance used as poison was found to be ORGANOPHOSPHORUS compounds(63%) readily available as Pesticides.Other substances included Pesticides such as Aluminium Phosphide, household cleaning items such as Phenyl,Medicines such as Benzodiazapines,TCA,Hair dye agents such as “Super Vasmol”, Kerosene and some unidentified/undetected substances as well.
• The most lethal poison was found to be Aluminium Phosphide.
• Symptoms-The most common symptoms were vomiting and restlessness and 28% of cases presented with a GCS of less then 10.
• Mortality-ICU and Hospital Mortality was 5 cases (9.09%), whereas 28 days mortality was 4 cases (7.27%) .

Discussion:

Poisoning is a major public health hazard. As per WHO, mortality rate attributed to poisoning in the year 2015 was 1.9 per 100000 population.As majority of poisoning are suicidal, it implies the ready availability of potentially poisonous substances such as pesticides and drugs. Stringent rules regarding their dispensing coupled with proper Government initiatives either through its organizations or through the help of NGO s could bring about a decline in Poisoning cases. People must be educated and counseled about deliberated poisoning and its aftermath which leaves behind a mental,physical,emotional and financial scar not only to self but also to the family,society and the country.

This is the first large descriptive study on the clinico-epidemiological profile and the treatment outcome of the poisoning cases from a tertiary care center of northeast India.

We intend to continue this study, follow up cases will be published with more details.

There is no conflict of interest with anyone.

No financial help is taken from anyone.

References:

1. https://nhp.gov.in/
2. www.who.int/ipcs/poisons/en
3. https://www.poison.org/poison-statistics-national
4. http://www.jflmjournal.org/article/S1752-928X(12)00107-2/fulltext
5. http://www.sciencedirect.com/science/article/pii/S1752928X12001072
6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982364/
7. http://apps.who.int/gho/data/view.main.SDGPOISON393v

Author:

1. Dr. DipankarHaloi, Fellow, Critical Care Medicine (IDCCM)
2. Dr. Apurba Kumar Borah, HOD, Critical Care and Emergency Medicine

The post Epidemiology and outcome of poisoned patient : A Retrospective analysis in a tertiary care hospital in northeast India appeared first on CCEM Journal.

Speaking of the clinical microbiology laboratory, the culture and sensitivity reports remains the mainstay for the successful recovery of the infected patient. Annual antibiograms made can help in the initial empiric treatment of the patient; these antibiotics can later be de-escalated based on the sensitivity reports. But how does one confirm that the reports are truly authentic? Validation of reports is the answer. This applies to not only for the microbiological, but also for the other departments of the laboratory as well.

Validationfor laboratory reports involves positive comparisonof results with an already approved method provided by a body or organization¹.

• Performance check of consumables: This check used for consumablesand instruments validates them while performing the test confirms to the basic standards. Ex: ATCC (American Type Culture Collection) strain checks of each and every prepared media and stains;temperature & calibration checks for centrifuge machines, refrigerators, incubators etc
• Method & reporting checks: Method used for the culture & reporting should be in strict adherence to the approved CLSI (Central Laboratory Research Institute) guidelines.
• Interlaboratorycomparison of results (ILC): Periodically, the reports of a lab should be compared to government approved laboratory (NABL); a quality improvement procedure.
• External quality assurance scheme (EQAS): There are certain government approved bodies which conduct exams for laboratories which are willing to maintain the quality of their reports. They send patient samples to these laboratories which they process and report back to them. Based on these results, they are given marks and are judged on the national (or international) scale. For microbiology in India, this body is at Sir Ganga Ram Hospital, New Delhi.

What if inspite of all the quality checks, the clinician is still at doubt with the reports?

• Disparity between the in vitro and in vivo results: This is the most common cause involved. In such a situation, the clinician must delve into its finer details.
  • Firstly, the immune mechanism where even though a sensitive antibiotic is administered, the patient deteriorates². Ex: Results of in vitro susceptibility testing cannot be expected to predict the clinical response to penicillin therapy in patients with group A streptococcal infection when the clinical outcome may be greatly influenced by TSS³. A similar disconnect can be seen with necrotizing pneumonia caused by community-acquired methicillin-resistant Staphylococcus aureus having the Panton-Valentine leukocidin (PVL) gene where patients may die of necrotizing pneumonitis despite receiving appropriate antimicrobial therapy⁴.
  • Secondly, the site of infection⁵: Certain antibiotics are more favorable to penetrate certain areas of the human body more than the others. For ex: 3rd generation cephalosporin have excellent CSF penetrability⁶.
  • Thirdly, the intrinsic factors^7,8,9:

1. A) Pharmacodynamicfactors such as beingbacteristatic or bactericidal; minimal inhibitory concentration; the relationship between the concentration of the drug and its antimicrobial effects and the post antibiotic effect (PAE)

and B) Pharmacokinetic parameters such as peak concentration (Cmax), the serum half-life (t1/2), and cumulative exposure to an antibiotic (areaunder-the-concentration-time curve [AUC]).

Bactericidal antibiotics are defined as being either concentration dependent (eg, aminoglycosides) or time dependent (eg, cephalosporins).  These effects may depend on the Cmax:MIC ratio ( aminoglycosides) or the AUC:MIC ratio (eg, fluoroquinolones). The goal of antimicrobial therapy with an aminioglycoside is to achieve a very high peak concentration, while that for a fluoroquinolone is to maximize drug exposure by achieving both a high peak and trough concentration. Other concentration-dependent antibiotics  includeazolides (ie, azithromycin), ketolides (ie, telithromycin), and vancomycin. Therefore, dosing becomes a critical factor in achieving the proper concentration-dependent bactericidal effect.Antimicrobial agents with time-dependent killing include beta-lactam agents (ie, penicillins, cephalosporins, carbapenems, and monobactams), macrolides, clindamycin, and oxazolidinones (ie, linazolid). Because these agents have minimal post antibiotic effect, the goal is to optimize the duration of exposure of the microorganism to antimicrobial concentrations above its MIC. On the other hand, there are some agents that appear to exhibit both concentration-dependent killing and time-dependent killing ; these include azithromycin, tetracyclines, vancomycin, and linezolid. For these agents, the AUC/MIC seems to be the primary parameter that correlates with clinical efficacy.

Prolonged in vivo PAEs are seen with antimicrobial agents that inhibit protein and nucleic acid synthesis such as  aminoglycosides and fluoroquinolones and they may be administered less frequently than would be predicted based on elimination half-life.

• Lastly, when the hesitation still remains on the validity of the reports , the clinician can, at best, send the samples can do an inter-laboratory comparison of the results. Care should be taken that both the samples are to be collected at the same time and source.

Validation of reports is primary for the better clinical outcome. The forementioned are just a few of the pillars of good quality practice in the laboratory. Without them, the reports are just as good as being invalid. For this purpose, in India, bodies like National Accreditation Board for Testing and Calibration Laboratories (NABL) have been established to assist the quality practicing laboratories. Therefore, the clinician should also be aware of these basic quality parameters being exercised in the laboratories whose reports they frequently refer to.

References:

1. Specific Criteria of Accreditation of Medical Laboratories (NABL 112; Issue No: 03, Issue Date: 01.02.2008, Amendment No: 03, Amendment Date: 16.10.2012). Available from: http://www.nabl-india.org/nabl/index.php?c=publicaccredationdoc&m=index&docType=both
2. Weinstein L, Dalton AC. Host determinants of response to antimicrobial agents. N Engl J Med 1968;279(9):467–73. McCormick JK, Yarwood JM, Schlievert PM. Toxic shock syndrome and bacterial super-antigens: an update. Annu Rev Microbiol2001;55:77–104.

3. Norrby-Teglund A, Thulin P, Gan BS, et al. Evidence for superantigen involvement in severe group A streptococcal tissue infections. J Infect Dis 2001;184(7):853–60.
4. Tseng MH, Wei BH, Lin WJ, et al. Fatal sepsis and necrotizing pneumonia in a child due to community-acquired methicillin-resistant Staphylococcus aureus: case report and literature review. Scand J Infect Dis 2005;37(6–7):504–7.
5. Kastenbauer S. Pneumococcal meningitis: a 21st century perspective. Lancet Neurol 2006; 5(2):104–5.
6. John CC. Treatment failure with use of a third-generation cephalosporin for penicillin-resistant pneumococcal meningitis: case report and review. Clin Infect Dis 1994;18(2):188–93.
7. Finch RG. Introduction: standards of antibacterial performance. ClinMicrobiol Infect 2004;10(Suppl 2):S1–5.
8. Craig WA. Basic pharmacodynamics of antibacterials with clinical applications to the use of beta-lactams, gycopeptides, and linezolid. Infect Dis Clin North Am 2003;17:479–501.
9. Drusano GL. Antimicrobial pharmacodynamics: critical interactions of ‘‘bug and drug.’’ Nat Rev Microbiol 2004;2(4):289–300.

Author:

Dr. Vicky Lahkar, Consultant Microbiologis (Narayna Superspeciality Hospital, Amingaon,Guwahati,Assam)

The post Validation of Culture & sensitivity reports appeared first on CCEM Journal.

Acute respiratory distress syndrome (ARDS), a clinical entity with a high mortality rate, requires aggressive ventilatory management. With a picture compounded with features of septic shock and multiorgan failure (MOF) the overall management becomes a huge challenge indeed. Timely intervention by the critical care team in the form of organ support, intensive invasive monitoring, control of sepsis and use of unique ventilatory strategies like prone ventilation can, however, help salvage some patients.

This was a K/C/O COPD, OSA, Post PCI, admitted with infective exacerbation of COPD, intubated in view of worsening ventilator parameters, developed severe ARDS and MOF managed successfully with prone ventilation and aggressive intensive care.

Case report:

A 65 years old male, K/C/O COPD, OSA, Post PCI, was brought to the Emergency Department with complaints of increased breathlessness associated with fever, chills and rigors for 1-2 days. He has been on domiciliary BiPAP. He also gave a history of allergy to Amoxicillin on reaching the ICU he was fully conscious, had tachycardia (HR 112 bpm), hypertensive (BP 180/90mmHg), respiratory rate of

24 /min, chest had bilateral wheeze on auscultation. Blood gas showed Respiratory alkalosis. His chest X ray did not show any obvious opacity. However, he was breathing with effort. He was put on intermittent BiPAP support. All battery of tests and cultures as per ICU protocol were sent promptly. As per the dynamic hemodynamic parameters, he was fluid resuscitated. Empirical broad-spectrum antibiotics administered. His Echocardiography was performed which showed an of LVEF 55% with no evidence of regional wall motion abnormality with a PASP of 55mmHg. Subsequent days patient showed no signs of improvement, HRCT chest was done which showed bilateral lower lobes and right middle lobe patchy areas of air space opacity with reticular interstitial thickening suggestive of infective etiology (possibility of atypical interstitial pneumonia can be considered).

Following day his general condition worsened, got intubated in view of hypoxia. Soon ventilatory parameters soared high. The P/F ratio being < 150; increasing PEEP & FiO2 requirement > 60%. With all this picture the call to PRONE the patient was taken. He was proned as per ARDS protocol, with low tidal volume of 6ml/kg (predicted body wt.) plateau pressure < 30cm H2O. His blood gases were closely being monitored, a Permissive Hypercapnia was maintained, keeping pH > 7.15. A high PEEP of 14-15 was set and Tidal volumes closely being followed. He was being Proned on an average of 16-18 hours a day. Post proning, his blood gases did show improvement yet the periods of time when he remained Supine, respiratory parameters worsened. He had to be proned multiple times as per protocol with needed number of hours being supined as neither chest X-ray nor Ventilator parameters improved. A suspicion of H1N1 was raised and markers for same were sent and empirically was started on Oseltamivir. Meanwhile his cultures were seen to be sterile. His H1N1 too was negative. Although he did not worsen, yet did not show much improvement either. After 5-6 days of proning regularly, his general condition and hemodynamics plummeted, and ventilator parameters increased. At this juncture the option of ECMO was thought of for the patient and the pros & cons of ECMO therapy were discussed to the relatives, however decision on same was pending. Fresh set of cultures were sent and antibiotics upgraded as per the hospital’s antibiogram, keeping hospital acquired infections in mind. Blood and the Endotracheal tube grew Klebsiella, antibiotics were modified as per sensitivity. His P/F ratio continued to be less than 150. No improvement in his lung imaging and ventilatory parameters remained high with increasing PEEP requirement.

After the 6^th time he was proned, his ventilator parameters started showing subtle changes of improvement. His P/F ratio started going beyond 200-250. His blood gas started improving. After the 10th days of ventilations, patient was tracheostomized with due consent from his first-degree kin. In subsequent days he showed improvement in his ventilatory parameters but the known complication of a prolonged ventilation with paralyzing agent and steroids critical illness myopathy, did set in by this time. He was not able to move his limbs at all. All the

ABG DIFFERENCES PRE-PONE AND POST-PONE

known sources of the same were discontinued. Mandatory physiotherapy continued. Within 1 week he started showing remarkable changes, being able to move his upper limbs and following days his lower limbs too. He was shifted to the step-down unit on a portable BiPAP support, which he tolerated well. When he was shifted to room. Regular physiotherapy follow-up was being done.

Discussion:

Recent studies report mortality of ARDS between 29% and 40% ¹. Institutions across the world, though, are experiencing a decline in the overall mortality, likely due to better general care for critically ill patients and, importantly, improved strategies of mechanical ventilation.

Prone ventilation has been extensively cited in literature in improving oxygenation in ARDS which was supported by the PROSEVA trail has shown the benefit in 28 days and 90 days mortality. The physiological mechanisms postulated are:

• Improvement in ventilation perfusion mismatch
• Recruitment of dependent lung areas
• Reduction in shunt
• Postural drainage
• Less compression of the lungs by the heart.

While prone ventilation cannot be recommended for routine ARDS treatment, a recent meta-analysis suggests improved outcomes using this approach in patients with severe ARDS.6 The ‘open lung’ approach calls for using higher levels of PEEP to keep alveoli open and prevent their collapse at end-expiration. A PEEP of 15 cm H2O, while prone, was reached in this case before attaining any oxygenation benefits and targeting the Pl pressure below 30 cm of H2O. High PEEP arm while

maintaining low tidal volumes during mechanical ventilation has been shown to improve oxygenation. Expertise is required in performing prone ventilation but at no additional cost. However, a patient in whom initial proning do not show improvement should always think of other optional treatment in the form of ECMO etc.

Conflicts of interest:

All authors have none to declare.

References:

1. Rubenfeld G.D., Caldwell E., Peabody E. Incidence and outcomes of acute lung injury. N Engl J Med. 2005; 353:1685–1693. [PubMed]

2. Erickson S.E., martin G.S., Davis J.L. Recent trends in acute lung injury mortality:1996–2005. Crit Care Med. 2005; 37:1574–1579. [PubMed]

3. Stapleton R.D., Wang B.M., Hudson L.D. Causes and timing of death in patients with ARDS. Chest. 2005; 128:525–532. [PubMed]

4. Dellinger R.P., Levy M.M., Carlet J.M. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock. Crit Care Med. 2008; 36:296–327. [PubMed]

5. Nanchal R., Jimenez E.J., Poalillo F.E. ALI, ARDS, and protective lung ventilation. In: Gullo A., Besso J., Lumb P.D., Williams G.F., editors. Intensive and Critical Care Medicine. 1st ed. Springer Verlag; Italy: 2009. pp. 207–216.

6. Alsaghir A.H., Martin C.M. Effects of prone positioning in patients with acute respiratory distress syndrome: a meta-analysis. Crit Care Med. 2008; 36:603–609. [PubMed]

7. ARDS Network High versus low positive end expiratory pressures in patients with acute respiratory distress syndrome. N Engl J Med. 2004; 351:327–336. [PubMed]

8. Poulakou G., Giamarellou H. Doripenem: an expected arrival in the treatment of infections caused by multidrug-resistant Gram-negative pathogens. Expert Opin Investig Drugs. 2008;17(5):749–771. [PubMed]

Author:

1. Dr. Sujan Dey, Consultant, Critical Care Medicine, Artemis Hospital, Gurugram, Haryana
2. Dr. Reshma Tewari, Director, Critical Care Medicine, Artemis Hospital, Gurugram, Haryana
3. Dr. Tina Jacob, Registrar, Critical Care Medicine, Artemis Hospital, Gurugram, Haryana
4. Dr. Amit Chawla, Registrar, Critical Care Medicine, Artemis Hospital, Gurugram, Haryana
5. Dr. Rati Bansal Goel, Senior Consultant, Critical Care Medicine, Artemis Hospital, Gurugram, Haryana

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Snakebite cases are not unusual to ED visit across the globe. Snakebite is an acute life-threatening time limiting medical emergency. It is a preventable public health hazard often faced by rural population in tropical and subtropical countries with heavy rainfall and humid climate. Although death due to snakebite is disproportionately low to the number of total bites partly because of bite by a non-venomous breed or dry bite (bites not accompanied by the injection of venom). Over 3000 species of snakes have been identified worldwide, with nearly 800 species considered venomous. In Indian subcontinent there are more than two hundred species of snakes out of which only about one-third will be venomous.

The three major families of venomous snakes are the Elapidae, the Viperidae, and the Colubridae Hydrophidae (WHO 2010).

Elapidae (cobra, king cobra, krait, and coral snake): Neuroparalytic toxin.

Viperidae (vipers): Vasculotoxic – Hemotoxic – bleeding disorder

Hydrophidae (sea snake): Though venomous, they seldom bite. Neuroparalytic toxin.

Whatever be the venom status of the biting snake all cases of such bite should get treated in a health care facility.

First aid and Transport of the victim

It aims to retard systemic absorption of venom and to prevent systemic effect of venom. It should be initiated as soon as the victim realizes about the bite before shifting to nearest medical facility. It is not mandatory to look for a fan mark to establish authentication of a bite.

Reassurance of the victim is important as it will ease the patient’s mental stress. Another important step in the pre-hospital setting is to immobilize the affected limb like in a case of a bone fracture. Any available rigid object can be used as a splint and to be tied with a roller bandage or a cloth. Nothing should be given orally. Traditional measures like tying a tourniquet or cutting and suctioning in an attempt to drain venom is to be discouraged. Patient should not be allowed to walk/run but should be passively transported as it will cause increased circulatory distribution of the venom. For every intervention adopted vital time should not be wasted.

Rapid clinical assessment and resuscitation

On arrival to the health care facility victim should be attended by a qualified physician with knowledge and experience to handle such cases. Many a times non-specific symptoms can lead to confusion because of anxious victim or bystanders. Definitive treatment with Anti-snake Venom (ASV) to be started as soon as signs of local/systemic envenomation begins. Hence knowledge of recognizing such signs and symptoms is necessary to efficiently treat such cases.

Symptomatic Patients

Neuroparalytic Venom mainly affects the neuro-muscular junction

Neuroparalytic snakebite patients present with typical symptoms within 30 min– 6 hours in case of Cobra bite and 6 – 24 hours for Krait bite. Although these time frame can vary significantly. These symptoms can be remembered as 5 Ds and 2 Ps.

5 Ds – Dyspnea, Dysphonia, Dysarthria, Diplopia, Dysphagia

2 Ps – Ptosis, Paralysis

Other signs are impending respiratory failure, diminished/lost tendon reflexes(DTR) and head lag.

Vasculotoxic toxidrome has both local and systemic manifestations. Locally there can be pain, swelling, blister formation or necrosis of the affected part. The swelling can be significant causing compartment syndrome. Hence surgical intervention is mandate early in the treatment as any delay can cause loss of the affected limb.

Systemic manifestation includes visible gingival bleed, epistaxis, ecchymosis, hematemesis, hemoptysis, hematochezia, sub-conjunctional bleed and bleeding from the bite mark per se. Acute abdominal pain can be attributed to gastro-intestinal or retro peritoneal bleed. Lateralizing neurological symptoms like asymmetrical pupils may point towards a Intra cranial bleed.

Life threatening complications are due to renal involvement. Patient presents with hematuria, hemoglobinuria, myoglobinuria followed by oliguria and anuria with acute kidney injury (AKI). Hypotension due to hypovolemia or vasodilatation or direct cardiotoxicity aggravates acute kidney injury. Long term sequelae e.g. pituitary insufficiency with Russell’s viper, Sheehan’s syndrome or amenorrhea in females.

Resuscitation and definitive urgent management should follow one the diagnosis is confirmed. The below mentioned are the red flag situations which require urgent resuscitation:

• Profound hypotension and shock resulting from direct cardiovascular effects of the venom or secondary effects such as hypovolemia, release of inflammatory vasoactive mediators, hemorrhagic shock or rarely primary anaphylaxis induced by the venom itself.
• Terminal respiratory failure from progressive neurotoxic envenoming that has led to paralysis of the respiratory muscles.
• Sudden deterioration or rapid development of severe systemic envenoming following the release of a tight tourniquet or compression bandage.
• Cardiac arrest precipitated by hyperkalemia resulting from skeletal muscle breakdown (rhabdomyolysis) after bites by sea snakes, certain kraits and Russell’s vipers.
• If the patient arrives late: Late results of severe envenoming such as renal failure and septicemia complicating local necrosis.

A very simple diagnostic tool: 20 mins whole blood clotting test (20WBCT) can give clue of hemolytic nature of toxin and warrants initiation of Anti-Snake Venom.

Anti-snake Venom (ASV)

Anti-snake venom is available is most of the health care facility where snake bite is prevalent. There is no absolute contradiction to ASV. Whenever indicated ASV should be started as soon as possible in indicated cases and has to be given in appropriate quantity. Commercially available ASV may be monovalent or polyvalent. In India polyvalent variant is only available which is effective against four common species; Russell’s viper, Common Cobra, Common Krait and Saw Scaled viper

ASV come in two forms: lyophilized powder and liquid. Lyophilized ASV is simply liquid ASV freeze-dried. Both the forms are equally potent in neutralizing venom. Advantage of lyophilized form against liquid is that the former has a longer shelf life and does not require a cold chain.

Dose of ASV:

ASV should be given only by the IV route, and should be given slowly, under supervision during the initial period to intervene immediately at the first sign of any reaction. The rate of infusion can be increased gradually in the absence of a reaction until the full starting dose has been administered. ASV must never be given by the IM route because of poor bioavailability by this route. Snakes inject the same dose of venom into children and adults. Children must therefore be given exactly the same dose of antivenom as adults. Epinephrine (adrenaline) should always be drawn up in readiness before ASV is administered.

Total ASV requirement ranges from 10 to 25 vials.

For neuroparalytic snakebite – ASV 10 vials stat as infusion over 30 minutes followed by 2nd dose of 10 vials after 1 hour if no improvement within 1st hour.

For vasculotoxic snakebite – Two regimens low dose infusion therapy and high dose intermittent bolus therapy can be used. Low dose infusion therapy is as effective as high dose intermittent bolus therapy and also saves scarce ASV doses.

Low Dose infusion therapy – 10 vials for Russel’s viper or 6 vials for saw scaled viper as stat as infusion over 30 minutes followed by 2 vials every 6 hours as infusion in 100 ml of normal saline till clotting time normalizes or for 3 days whichever is earlier.

Or

High dose intermittent bolus therapy – 10 vials of polyvalent ASV stat over 30 minutes as infusion, followed by 6 vials 6 hourly as bolus therapy till clotting time normalizes and/or local swelling subsides.

No ASV for Sea snakebite or pit viper bite as available ASV does not contain antibodies against them.

Adverse Anti Snake Venom Reactions Anaphylactic reaction to ASV is not managed correctly it can be treated in

an uncommon occurrence. However, if even remote health care facility. Early anaphylactic reactions occur within 10–180 min of start of therapy and is characterized by itching, urticaria, dry cough, nausea and vomiting, abdominal colic, diarrhea, tachycardia, and fever. Some patients may develop severe life-threatening anaphylaxis characterized by hypotension, bronchospasm, and angioedema.

Pyrogenic reactions usually develop 1–2 h after treatment. Symptoms include chills and rigors, fever, and hypotension. These reactions are caused by contamination of the ASV with pyrogens during the manufacturing process.

Late (serum sickness–type) reactions develop 1–12 (mean 7) days after treatment. Clinical features include fever, nausea, vomiting, diarrhea, itching, recurrent urticaria, arthralgia, myalgia, lymphadenopathy, immune complex nephritis and, rarely, encephalopathy.

At the first sign of a reaction we have to stop the ASV immediately. Administer Epinephrine (adrenaline) (1 in 1,000 solution, 0.5 mg (i.e 0.5 ml) in adults intramuscular over deltoid or over thigh; In children 0.01 mg/kg body weight) for early anaphylactic and pyrogenic ASV reactions. Ideally 2 syringes should be drawn up ready if the ASV is known to cause frequent reactions. Administer chlorpheniramine maleate 10 mg intravenously.

Late Serum sickness reactions can be easily treated with an oral steroid such as prednisolone, adults 5mg 6 hourly, oral H₁ antihistamines provide additional symptomatic relief.

Neurotoxic Envenomation

Antivenom treatment alone cannot be relied upon to save the life of a patient with bulbar and respiratory paralysis. Neostigmine is an anticholinesterase that prolongs the life of acetylcholine and can therefore reverse respiratory failure and neurotoxic symptoms. It is particularly effective for post synaptic neurotoxins such as those of the Cobra. There is some doubt over its usefulness against the pre-synaptic neurotoxin such as those of the Krait and the Russell ’s viper. However, it is worth trying in these cases. In all cases of neurotoxic envenomation, the “AN challenge Test” to be undertaken: Atropine 0.6mg followed by neostigmine (1.5mg) to be given IV stat and repeat dose of neostigmine 0.5 mg with atropine every 30 minutes for 5 doses. A fixed dose combination of Neostigmine and glycopyrrolate IV can also be used. Thereafter to be given as tapering dose at 1 hour, 2 hour, 6 hours and 12 hour. Majority of patients improve within first 5 doses. Patient need observation closely for 1 hour to determine if the neostigmine is effective. After 30 minutes, any improvement should be visible by an improvement in ptosis. Positive response to “AN” trial is measured as 50% or more recovery of the ptosis in one hour.

Renal Failure and ASV

Renal failure is a common complication of species such as Russell’s Viper. The contributory factors are intravascular hemolysis, DIC, direct nephrotoxicity and hypotension and rhabdomyolysis. Such patient will require renal replacement therapy.

Antibiotics and Tetanus Prophylaxis

Broad spectrum antibiotic coverage along with post exposure tetanus prophylaxis.

Debridement of Necrotic Tissue

Cellulitis and Compartment syndrome needs urgent surgical intervention and require surgeon opinion.

Follow-up

A snakebite victim discharged from the hospital should continue to be follow up. At the time of discharge patient should be advised to return to the emergency, if there is worsening of symptoms or signs such as evidence of bleeding, worsening of pain and swelling at the site of bite, difficulty in breathing, altered sensorium etc. The patients should also be explained about the signs and symptoms of serum sickness. (fever, joint pain, joint swelling) which may manifest after 5-10 days.

Reference:

Management of Snake Bite- MOH Government of India

Author:

Dr. Soumar Dutta, Consultant & Coordinator, Emergency Medicine (Narayana Superspeciality Hospital, Kamrup, Assam)

The post Snake Bite Protocol – An Indian Perspective appeared first on CCEM Journal.

The first case of extra pontine myelinolysis was described in 1987 and before that the concept of central pontine myelinolysis was being widely used. When extra pontine myelinolysis and central pontine myelinolysis occur simultaneously it is known as the osmotic demyelination syndrome. The etiology of extra pontine myelinolysis is most commonly a metabolic insult to the brain in the form of over or rapid correction of hyponatremia (a change in serum sodium more than 25mmol/litre within 48 hours). Moreover it is said that some predisposing factors attribute to its severity like Alcoholism, Malnourishment, Sepsis, Severe burn, SIADH, Chest infection etc. Extra pontine myelinolysis is more commonly found in chronically hyponatremic patients in whom it occurs 7-14 days after acute osmotic shift. This report describes a 57 years old male with extra pontine myelinolysis with history of rapid correction of hyponatremia who presented with acute parkinsonian symptoms.

Case Report:

A 57 years old male, known case of type 2 diabetes mellitus and hypertension had history of multiple episodes of vomiting 15 days back before coming to our hospital. He was admitted in a local hospital where on biochemical evaluation his serum sodium was found to be 104 mmol/lit which was corrected to 130 mmol/lit within 24 hours. The patient was improving and was being discharged after a 5 day stay in the hospital. Then after 2-3 days the patient developed tremors of hands and tongue, dysarthria and stiffness of limbs. After admission to our hospital, on doing laboratory investigation he was found to have dyselectrolytemia which were corrected accordingly. On neurological examination the patient followed simple commands; cog wheel rigidity was positive. GCS was found to be E4V3M5. MRI brain was done which showed features suggestive of extra pontine myelinolysis. The clinical features along with MRI findings led the patient to be diagnosed as a case of extra pontine myelinolysis with acute Parkinsonian symptoms. He was managed in our set up conservatively. Physiotherapy training was given and the patient was gradually improving and was discharged by explaining the nature of the illness to the patient party.

Discussion:

Extra pontine myelinolysis is a rare, acute, demyelinating process that involves the areas of the brain outside the pons. It is most commonly found in association with central pontine myelinolysis which involves the pons. When osmotic demyelination occurs, it can be lethal as it is usually irreversible and has no proper management. Thus prevention is the key. It is generally suggested that the rate of correction of serum sodium should not be more than 1-2mmol/litre/hour during first few hours and not more than 8-10mmol/lit in first 24 hours.

Rapid correction of acute hyponatremia causes rapid osmotic shifts of fluid which leads to hypernatremia and eventually shrinkage of brain cells and demyelination. When hyponatremia develops gradually that is in chronic hyponatremia the brain cells can compensate by decreasing intracellular osmolarity through the loss of osmolytes and thereby limiting neurologic dysfunction. So during rapid correction of chronic hyponatremia, the regeneration of these osmolytes lag and cerebral dehydration occurs. Microscopically the lesion shows loss of oligodendrocytes with preservation of axons unless the lesion is highly advanced. It may involve the basal ganglia, thalamus, cerebellum and subcortical white matter. On MRI, T2 weighted image shows trident shaped signal changes. In our case, the history of low sodium with subsequent rapid correction, the clinical symptoms and the basal ganglia changes in MRI were strongly in favour of extra pontine myelinolysis. Extra pontine myelinolysis may manifest as postural limb tremors, myoclonic jerks, parkinsonian presentation, dystonia, catatonia or pyramidal dysfunction. Whatever may be the cause of hyponatremia whether acute or chronic, it has to be corrected slowly.

Conclusion:

In conclusion, hyponatremia may be the manifestation of various disorders. However osmotic demyelination is preventable if we correct serum sodium level slowly and if the correction is with hypertonic saline we should monitor serum sodium frequently.

References:

1. Dr.Mohan, D.Kashinkunti, Dhananjaya M; Extra pontine myelinolysis- A case report; Scholars journal of applied medical sciences; 2013;1[5]:527-529
2. RJ Martin; Central and extra pontine myelinolysis; The osmotic demyelination syndrome; J Neurology Neurosurgery. Psychiatry 2004
3. Ming-Tsung Hsu, Wai-Mau Choi; Extra pontine myelinolysis —A case report; J Emergency critical care medicine; Vol.19, no-4, 2008
4. John K. Mcilwaine; Howard L. Corwin; Textbook of critical care, Eith edition pp53-55

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