We are located in Garo Hills. Garo Hills is part of the State of Meghalaya. It is mainly inhabited by the people of the Garo Tribe. In terms of Medical Care it is one the most backward parts of the North East.

The major challenges are:

• Poor connectivity  and distance( Some areas  are completely in access able during the monsoons)
• Poorly operated Primary Health Centres
• Lack of medical professionals.

With the bulk of medical professionals seeking to be located in towns the major gap in the health care has been in the rural areas.

Need for Critical Care in the Rural:

The major population in any community is rural. The lack of health literacy, distance and transportation, social stigma and belief in traditional medication, patients are very often brought acritically ill. This has created an unpreceded demand for Critical Care Services. With little to no basic facilities at the Primary Health Centres the critically ill patients often succumb or are referred.

Experience of Critical Care in a rural setting:

The need to support the Medical work by providing cost effective and high quality health care in rural Garo Hills has been the primary goal of Garo Hills Adventist Mission Nursing Home. The Nursing Home is located in a small village called Jengjal, West Garo Hills A junction with accessible roads to all parts of Garo Hills.

It has been over 15 months since the Nursing Home has been established and we have been able to see how a basic knowledge in Critical Care can be lifesaving and very rewarding.

The team consists of two Paediatricians, a Gynaecologist, a Dentist supported with 4 nurses. The Nursing Home is a 10 bedded facility. The ER is a 5 bedded set up which has basic facilities eg,Cardiac Monitor, ECG machine and oxygen.

With being the only institution outside the main town providing specialised care in Paediatrics and Obstetrics and Gynaecology, a good number of patients present critically ill.

The most common critically illness cases are Acute Myocardial Infartion, Hypertensive Emergencies, Septic Shock,  Status Asthmaticus, Anaphylactic Shock , foreign body in the ear, Snake Bites, Insect Bites, Renal Colic, croups, Status Epilepticus  and in OBGYN Eclampsia.

It has been our experience that with a basically equipped ER, a standard emergency management protocol and a trained medical team many of the most commonly encountered emergencies can be treated well even at a rural Health care centre.

Author:

Dr. Denyl Avinash Joshua
Medical Director
Garo Hills Adventist Mission Nursing Home
Jengjal, West Garo Hills
Meghalaya

The post Critical Care Medicine in a Rural Setting appeared first on CCEM Journal.

Hypoglycemia is a very common side effect of insulin therapy and oral hypoglycemic agents. Occurrence of cardiac arrest as a result of severe hypoglycaemia has not been documented much in literature. We describe a interesting case of a type 2 diabetic patient admitted in intensive care unit following traumatic brain injury having cardiac arrest resulting from hypoglycaemia. A 59 years old type2 diabetic patient was transferred to our intensive care unit from a nearby hospital with history of traumatic brain injury for which decompressive craniotomy followed by duroplasty had already been done. His random blood sugars were uncontrolled for which he was on Insulin infusion as per our hospital protocol. He suffered cardiac arrest (asystole) at night for which no apparent cause could be identified except very low random blood sugar (<30mg/dl).

Case report:

A 59 years old type 2 diabetic and hypertensive patient was transferred to our intensive care unit from a nearby hospital with history of traumatic brain injury for which decompressive craniotomy followed by duroplastyhad  been done. Tracheostomy was already done in the previous hospital but he needed ventilator support. At admission his GCS was E4M1VT. Otherwise he was hemodynamically stable.  His random blood sugars were uncontrolled for which he was oncontinuous Insulin infusion as per our hospital protocol. After two days of admission at around 5;45 AM he developed cardiac arrest and CPR was started according to ACLS protocol.  The blood sugar were found to be very low( <20 mg/dl) . Patient revived after getting 100 ml 25% dextrose, 1 mg Epinephrine. Post cardiac arrest care was provided. During the post cardiac arrest analysis no apparent cause could be found except Low plasma glucose. So the cardiac arrest was attributed to hypoglycaemia.

Discussion:

Acute hypoglycaemia provokes pronouncedpatho- physiological responses, the important consequences of which are to maintain the supply of glucose to brain and promote hepatic production of glucose. Blood flow is increased to the myocardium, splanchnic circulation and the brain. Hypoglycemia and the rapid changes in blood glucose have been shown to increase counter-regulatory hormones such as epinephrine and nor-epinephrine, which may induce vasoconstriction and platelet aggregation, thereby precipitating myocardial ischemia. Autonomic activation principally of the sympatho-adrenal system, results in end-organ stimulation and the profuse release of epinephrine which precipitates hemodynamic changes like tachycardia, increased peripheral systolic blood pressure, decreased central blood pressure and increased myocardial contractility with an increased ejection fraction3.
The catecholamine induced myocardial contractility may induce ischemia in the myocardium in patients with CAD. The greater oxygen demand is not met because of not only the rigid vessels, but also endothialialdyrsfunction with failure to vasodilate.

There have been multiple case reports associating angina with hypoglycaemia. ECG changes, including ectopic activity, flattening of T-wave, ST depression, ventricular tachycardia, and atrial fibrillation, have been reported in cases of low plasma glucose1.

Evidence is accumulating that severe hypoglycaemia can provoke adverse cardiovascular outcomes such as myocardial ischemia or cardiac arrhythmia like torsade 2. Episodes of severe hypoglycaemia are common during intensive therapy in type-1 and type-2 diabetes in the out-patient as well as in-patient setting. The challenge to the physician is to lower blood glucose to normal values to decrease the risk for long-term complications and at the same time minimize hypoglycaemia and hypoglycaemia-assosiated morbidity and mortality.

Conclusion:

Although not included in AHA guidelines as a cause of cardiac arrest (5H&5T), we believe hypoglycaemia can cause cardiac arrest independently and in this case after thorough investigation no other cause could be found except hypoglycaemia. So we strongly suggest hypoglycaemia can independently cause cardiac arrest and should be considered as a cause of cardiac arrest.

References:

1. Severe Hypoglycemia May Lead to Fatal Arrhythmia – Medscape – Aug 23, 2013.
2. Hannoodi F, Alwash H, Shah K, Ali I, Kumar S, Zakaria K. A Case of Hypoglycemiainduced QT Prolongation Leading to Torsade de Pointes and a Review of Pathophysiological Mechanisms. Clinics and Practice. 2017;7(3):960. doi:10.4081/cp.2017.960.
3. Chopra S, Kewal A. Does hypoglycemia cause cardiovascular events? Indian Journal of Endocrinology and Metabolism. 2012;16(1):102-104. doi:10.4103/2230-8210.91203.

Author:

Dr.AkashBaruah, Intensivist
Narayana Superspeciality Hospital, Guwahati, Assam

The post Hypoglycemia as an independent cause of cardiac arrest: A case report 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.

Bartter’s Syndrome is characterized by renal potassium wasting with hypokalemia, metabolic alkalosis, increased renin-angiotensin-aldosterone system, normal blood pressure, resistance to the pressor effects of angiotensin II and juxtaglomerular cell hyperplasia. Most of the cases have been noted in the pediatric age group and adult-onset cases are very rare. In 1962, Frederic Bartter and his colleagues wrote their seminal paper based on two patients with hypokalaemic metabolic alkalosis, hyperaldosteronism, normal blood pressure, decreased pressor responsiveness to angiotensin II infusion and hyperplasia of the juxtaglomerular apparatus.The syndrome comprising the above mentioned observations was hence named after him. We report a case of adult-onset Bartter’s syndrome.

Case Report :

A 52 year old Gentleman with past history of Pulmonary Koch came with breathing difficulty along with fever.In view of severe respiratory distress, he was intubated and put on Mechanical Ventilation and treatment initiated after sending all relevant investigations.From history and from past medical records it was found that he was Normotensive in matters pertaining to his Blood Pressure.Initial  routine investigations revealed low serum Potassium levels for which intravenous Potassium Chloride was given. Despite correction,his serum Potassium did not rise and maintained in the range of 2.4-2.9 mEq/L.Hence cause for persistent hypokalemia was evaluated and Arterial Blood Gas analysis which was already being done to asses ventilatory status, correlated to look for any respiratory cause of hypokalemia.ABGs showed relatively persistent Metabolic Alkalosis.Obvious cause of Metabolic Alkalosis such as diueretics,renal failure were also ruled out.Ultrasonography of Abdomen revealed tiny Right renal calculi, hypoechoic  areas in bilateral Adrenal glands and Common Bile Duct Stone.In view of renal stone, urinary Calcium was evaluated which was found to be high.Suspecting Bartter Syndrome as the above mentioned findings pointed towards it, his serum Aldosterone level was assessed which was also high.Serum Renin levels were not assayed due to Laboratory constraints.Adrenal Biopsy was planned after patient stabilization in view of ?Adrenal Mass.Renal Biopsy was also not done.Meanwhile the patient was tracheostomised due to difficult weaning and subsequently the patient expired.

Discussion:

The constellation of Hypokalemia, Normotension, Metabolic Alkalosis, increased Aldosterone level and increased Urinary Calcium substantiated thedifferential  diagnosis of Bartter’s syndrome.However, as stated, Renin Activity could not be assesed and Renal Biopsy was not done.Also since Adrenal gland biopsy could not be done,an Adrenal glandtumour contributing to increased serum Aldosterone and hypokalemia could also be not ruled out.Hence  the possibility of any other differential diagnosis contributing to the above constellation of findings  is open for debate. Terms such as Bartter‐like syndrome do little to help the clinician identify the specific metabolic defect and treat the patient’s illness correctly. It may be better to sub‐classify Bartter syndrome by renal pathophysiological abnormality. By this method, Bartter syndrome falls into four subgroups: (i) antenatal Bartter syndrome (hyperprostaglandin E2 syndrome); (ii) the Gitleman variety of Bartter syndrome (Gitleman syndrome); (iii) classical Bartter syndrome; and (iv) pseudo‐Bartter syndrome.Often while assessing a cause of Hypokelemia we might miss that the hypokalemia  might represent anyone of the  constellation of findings correlating with any above mentioned syndrome.Bartter’s syndrome may be mimicked by magnesium deficiency, diuretic use or vomiting. Magnesium depletion causes kaliuresis, diuretics cause potassium and volume depletion and vomiting causes renal potassium wasting and volume depletion.The primary aim of the treatment of the Classical Bartter syndrome is correction of hypokalaemia and alkalosis. Therefore administration of potassium chloride is always necessary. The dose of KCl supplementation should individually be titrated in accordance to the patient’s needs and must balance the amount lost by the kidney. However, this mode of supplementation therapy is almost totally ineffective by itself, since administered potassium is lost through the kidney in a short period of time. It may seem logical that potassium‐sparing agents such as spironolactone  would be aneffective additiveto supplementation therapy at this stage. Indeed these groups of medication offer an effective but transient control of hypokalaemia.The most beneficial group of medication in treatment of classical Bartter syndrome is the prostaglandin synthetase inhibitors. Indomethacin (2–5 mg/kg/day), acetylsalicylic acid(100 mg/kg/day), and ibuprofen (30 mg/kg/day) have all been tried. But the most frequently used is indomethacin.

Conclusion:

Although rare a strong suspicion for this syndrome should be there while dealing with difficult cases of hypokalemia.

REFERENCES:

1. Bartter FC, Pronove P, Gill JR, Jr, MacCardle RC. Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis:a new syndrome. Am J Med. 1962;33:811. [PubMed]
2. Tomko DJ, Yeh BPY, Falls WF., Jr Bartter’s syndrome, Study of a 52-year-old man with evidence for a defect in proximal tubular sodium resorption and comments on therapy. Am J Med. 1976;61:111.[PubMed]
3. Gans ROB, Hoorntje SJ. Bartter’s syndrome. In: Cameron S, Davison AM, Grünfeld JP, Kerr D, Ritz E, editors. Oxford textbook of clinical nephrology. P. 782. Oxford University Press; 1992.
4. White MG. Bartter’s syndrome. Arch Intern Med. 1972;129:41. [PubMed]
5. Schöter J, Timmermans G, Sexberth HW, Greven J, Bachmann S. Marked reduction of Tamm-Horsfall protein synthesis in hyperprostaglandin E-syndrome. Kidney Int. 44:401, 1993. [PubMed]
6. Strokes JB. Effect of prostaglandin E2 on chloride transport across the rabbit thick ascending loop of Henle. Selective inhibition of the medullary portion. J Clinn Invest. 1979;64:495. [PMC free article][PubMed]
7. Halushka PV, Wohltmann H, PriviteraPj, Hurwitz G, Margolius HS. Bartter’s syndrome: urinary prostaglandin E-like material and kallikrein; Indomethacin effects. Ann Intern Med. 1977;87:281.[PubMed]
8. Stein JH. The pathogenetic spectrum of Bartter’s syndrome. Kidney Int. 1985;28:85. [PubMed]
9. Bartter FC. On the pathogenesis of Bartter’s syndrome. Miner Electrolyte Metab. 1980;3:61.
10. Baehler RW, Work J, Kotchen TA, McMorrow G, Guthrie G. Studies on the pathogensis of Bartter’s syndrome. Am J Med. 1980;69:933. [PubMed]

Author:

Dr. Dipankar Haloi, Fellow, Critical Care Medicine (IDCCM)

The post A Case of Adult-Onset Bartter’s Syndrome appeared first on CCEM Journal.

The International Society of Parenteral Nutrition (ISPN), had been founded in 1966 to discuss the scientific work arising from the rapid development in Europe of parenteral nutrition in the late 50s and early 60s.The spreading interest in parenteral nutrition in the US in the 60s eventually led to the establishment of the American Society of Parenteral and Enteral Nutrition (ASPEN) in 1977.ISPN had to redefine its role to better target the needs of those involved in clinical nutrition in Europe and it was decided that there was a need for a scientifically-orientated organization providing a common ground for European scientists from many disciplines involved in nutritional support. So ESPEN had been founded in 1980.

Since 1997, ESPEN publishes guidelines and position papers on a regulatory basis in Clinical Nutrition. In 2006 ESPEN Guidelines on adult enteral nutrition came.  These guidelinesdo provide evidence-based information about specific problems like timing, dosing, composition androute of application. They also show where additional studies are needed and under which conditions limitation or withdrawal of nutritional supportlike other therapies might be adequate.

Earlier blederised feed was given to patients those are not able to eat, for that we required a liquid secession and a lot of other things to maintain quality.We knew that the use of blenderized formula for enteral nutrition can lead toinconsistent and imprecise delivery of macro and micro nutrients (1, 2, 3),thus exposing patients to the risk of bacterial infection (1, 5).The use of “natural” food in blenderized formulas causes amajor variance in nutrients and bacterial contamination ascompared to reconstituted industrial powder formulas ormodular formulas.(1)After that formula feed started to reduce infection.(6)

Continuous feeding took place of bolus feeding to improve tolerance level and to achieve better nutritional goal.And now ready to hang is available in developing countries to ease nutritional support in critical care. (12) Now implementation is easy as compare to earlier.

In developing country most of the hospitals don’t have liquid secession where feed can prepare for patients to give continuous feeding to hang more than 4 hours (11). As we knew that with bolus feeding other problems are there like intolerance, more nursing time, less achieve nutritional goal, less hygienic(11,12,15,16).

So ready to hang is the only option but this is costly. Here I am sharing a plan to resolve all this.

• We need a SOP for all patients to maintain equal quality.
• We need SOP for Nutritional Screening andAssessment.
  • All ICU admissions, should be screened to assess their need for nutrition support.(17,18,19,20,21) Recommend nutrition support within 24 to 48 hours of ICU admission (or once hemodynamically stable) for:
    • Undernourished or hypercatabolic patients (18-20).
    • Ill patients expected to stay in ICU for 3 days or more (20).
    • Patients not expected to commence diet within next 5 days or more (17).
  • A ‘nutrition risk in the critically ill score’ (NUTRIC Score) has recently been validated for screening ICU patients. Further validation studies are needed (22).
• SOP for starting feed (TPN/EN), where we can use ESPENguidelines
  • EN should start within 24 hours.(10)
  • A PEG tube may be utilized for feedings withinseveral hours of placement:current literaturesupports within 2 hours in adults and 6 hours in infants and children. (13)
  • All patients who are not expected to beon normal nutrition within 3 days should receive PN within24–48 hour if EN is contraindicated or if they cannot tolerate EN.(9)
• SOP for calculating nutritional requirement.
  • 25 to 35 Kcal/Kg body weight /day or BEE(Basal Energy Expenditure) * Injury Factor
  • 2 to 2 gm / Kg body weight /day.
• SOP to achieve nutritional goal in first 24 hours.
  • 80 % nutritional requirement needs to achieve in first 24 hours.
• SOP to give special formulas like glutamine, L- arginine, omega 3 fatty acid, zinc etc(17, 19, 21, 23, 24).
• We need to make a Nutrition Support Team (NST) to update SOP and giving training and keeping an eye on implementation of these policies etc.

This is action plan for tube feeding patients which is best suitable for limited resources hospital:

REFERENCES:

1. CristhianeMitne, R.D.; Ana Maria Gomes Simões, R.D.; Débora Wakamoto, R.D.; Giselle Pedral De Liori, R.D.; Mary Sullivan, M.P.H., R.D.; Gail M. Comer, M.D. Analysis of Blenderized Enteral Diets. Journal of Clinical Nutrition, 2001, volume 16, pg 100-109.
2. Anderton A. Reducing bacterial contamination in enteral tube feeds. Br J Nurs 1995; 4:368-77.
3. Tanchoco CC, Florentino RF, Castro MCA, Belmonte BN, Natividad AS. Survey ofblenderized diets prepared by some hospitals in metro Manila: Phase II. Nutrient composition of blenderized diets. Hospital Journal 1990; 2:17-26.
4. Anderton A. The potential of Escherichia coli in enteral feeds to cause food poisoning: A study under simulated ward conditions. J Hosp Infect 1984; 5:155-63.
5. Schroeder P, Fisher D, Volz M, Paloucek J. Microbial contamination of enteral feeding solutions in a community hospital. JPEN 1983; 7:364-8.
6. Gallagher-Allred CR. Comparison of institutionally and commercially preparedformulas. Nutritional Support Services 1983; 3:32.
7. Gibbs J. Bacterial contamination of nasogastric feeds. Nursing Times 1983; 79:41-7.
8. Heyland DK, Dhaliwal R, Jiang X, Day AG. Identifying critically ill patients who benefit the most from nutrition therapy: the development and initial validation of a novel risk assessment tool. Critical Care. 2011; 15(6):R268.
9. Singer et al. ESPEN Guidelines on Parenteral Nutrition: Intensive care/ Clinical Nutrition 28 (2009) 387–400.
10. G. Kreymann et al. ESPEN Guidelines on Enteral Nutrition. Clinical Nutrition (2006)25, 210–223.
11. Bankhead et al. Enteral Nutrition Practice Recommendations/Powdered, reconstituted formula, HBM, and EN formula with additives should have a 4-hourhang time. (C)Journal of Parenteral and Enteral Nutrition / Vol. 33, No. 2, March/April 2009.
12. Bankhead et al. Enteral Nutrition Practice Recommendations/ Closed-system EN formulas can hang for 24-48hours per manufacturer’s guidelines. (A) Journal of Parenteral and Enteral Nutrition / Vol. 33, No. 2, March/April 2009.

Author:

Dr. Shabista Nasrin (Clinical Dietician & Nutritionist, Narayana Superspeciality Hospital, Guwahati)

The post Implementation of Nutritional Guidelines for Critical Care Patients in Developing Countries appeared first on CCEM Journal.

Introduction: The reported incidence of acute kidney injury after rhabdomyolysis is as high as 65%¹ which occurs as a result of multiple mechanisms including tubular obstruction, direct and ischemic tubular injury, or intrarenal vasoconstriction. In this report, we present a case of acute kidney injury induced by rhabdomyolysis in a young male post-trauma.

Presentation: A 37 yr old male patient presented to the emergency department with a history of trauma and physical assault 4 days back, multiple wounds all over the body and reduced urine output for 1 day. On examination he was found to have generalised swelling all over the body, multiple bruises and abrasions along with fracture of right 4^th metatarsal bone. Laboratory studies revealed CPK: 17345 IU/L; BUN: 79mg/dl; Serum creatinine: 11.35mg/dl; Serum potassium: 4.1meq/L; Urine Ph: 5. Adequate hydration was started with balanced salt solution and 0.9% NS also haemodialysis was done with which the patient’s renal functions improved gradually.

Conclusion: Rhabdomyolysis induced AKI in a patient with no co morbidities resolves gradually with adequate hydration and urine output monitoring.

Introduction:

Rhabdomyolysis is a clinical condition in which skeletal muscles break down rapidly releasing toxic substance like creatine kinase and myoglobin into the blood stream which in turn leads to kidney injury. This can happen because of sustained trauma, sepsis, heat stroke or even drugs.

Pathophysiology:

Rhabdomyolysis involves direct sarcolemic injury leading to depletion of ATP within the myocyte which impairs the function of ATPase pump. This causes an increased sarcoplasmic calcium levels leading to a state of persistent contraction of the myofibril. This sustained contraction leads to further energy depletion.

After myocyte injury, intracellular contents are released into the circulation.^{2, 3}   Hyperkalaemia, hyperuricaemia, and hyperphosphataemia can develop rapidly. High levels of phosphate released in blood; bind to calcium, and calcium–phosphate deposition occur in soft tissue, resulting into hypocalcaemia. Ischemic muscle is also forced to utilise anaerobic metabolism leading to metabolic acidosis.

During the recovery phase of rhabdomyolysis, significant number of patients develop hypercalcaemia, due to the release of vitamin D stores from injured muscle, providing substrate for the production of excess 1,25-dihydroxyvitamin D^4.  Hypercalcaemia may be further exacerbated if excess calcium is administered during the acute hypocalcaemic phase.

Myoglobin a dark red haem-containing protein stores and transports oxygen in muscle. Only small levels of it are normally present in plasma. It has a small molecular weight and is easily filtered. When the renal threshold for free myoglobin is exceeded it appears in urine.⁵ This then interacts with the Tamm–Horsfall proteins to form brown granular casts resulting in tubular obstruction. The process is favoured when the urine is acidic and may have no nephrotoxic effect when the urine is alkaline.

Myoglobin also causes deficit of nitric oxide leading to renal vasoconstriction which further compounds to kidney injury. Renal blood flow is further compromised by hypovolaemia, activation of the renin–angiotensin system, and additional vascular mediators. ²

Clinical features:

Severity of symptoms depends upon the degree of muscle damage and extent of kidney injury. Rhabdomyolysis may be asymptomatic or associated with muscle pain, nausea, sepsis, dyselectrolytemia, arrythmia, acute renal failure and even coma. A high degree of suspicion is needed from prompt management and avoidance of complications arising. Severe pain may at times limit limb movement and additionally in compartment syndrome or crush injury the muscles may get tense and swollen, leading to a sensoryneural loss. In diffuse muscle injury such as which occurs with drugs, there may be a generalised malaise with diffuse myalgia. Rarely, patients may volunteer that their urine has changed to a red or brown colour.

Lab findings:

Rhabdomyolysis is typically diagnosed when the CK is more than 5000 units/litre or five times its normal upper limit. Myoglobin levels peak before increases in CK, however, myoglobin is metabolised rapidly at sites outside of the kidney hence CK a more reliable marker of rhabdomyolysis. The absence of myoglobinuria does not rule out the possibility of rhabdomyolysis. In a study of 475 patients with rhabdomyolysis diagnosed by CK levels, myoglobinuria was only detected in 19%⁶  A Metabolic Acidosis with high anion gap is usually observed. Arterial blood gases also reveal trend of serum lactate and pH and serves as a guide for fluid replacement. Regular observations including hourly urine output are required to detect any deterioration promptly.

Case Report:

A 37 year old male, with no comorbidities, presented to the emergency department with complains of reduced urine output for 1 day, there was an associated history of physical assault 4 days back in which he suffered multiple contusions and abrasions all over his body along with a  fracture of right 4^th metatarsal bone, for which orthopaedic consult was taken. He was admitted to the critical care department and his initial laboratory studies revealed CPK: 17345 IU/L, BUN: 79mg/dl, Serum creatinine: 11.35mg/dl, Serum Potassium: 4.1meq/L, Urine Ph: 5, Serum Calcium: 7.2mg/dl, Serum Phosphorus: 7.6mg/dl.

Foley’s catheterization was done and central venous access was taken. Keeping myogologinuria induced rhabdomyolysis in mind he was thereafter managed primarily with fluid resuscitation with a target urine output of 3 ml/kg/hr or 300 ml/hr. 0.9% Normal saline, balanced salt solution was used while monitoring potassium and arterial blood gases to look for hyperchloraemic acidosis.

Continuous infusion of soda bicarbonate was initiated to alkalinise the urine to reduce the precipitation of Tamm–Horsfall protein complexes. A urinary pH of 7 was achieved on day 2 of the treatment. We also initiated infusion of Inj furosemide at 5-10 mg/hr to maintain an adequate urine output.

The patient was evaluated by a nephrologist and haemodialysis was initiated on day 2 and day 4 of admission, soda bicarbonate and furosemide was gradually tapered off with close monitoring of urine output. Fluid resuscitation continued, as guided by IVC dimensions. The patients renal functions improved gradually and he was later discharged in a stable condition with adequate urine output, with a serum creatinine of 2.59mg/dl and CPK: 150 IU/L.

Discussion:

We have reported a case of Acute kidney injury due to trauma induced rhabdomyolysis, patient here landed up into AKI due to dehydration and inadequate fluid resuscitation, which eventually resolved with intravenous hydration therapy. Another contributing factor of adequate recovery was young age of the patient with no history of any comorbidities or drug intake which could have been be a secondary cause of renal dysfunction.

Evidence for the use of sodium bicarbonate as a therapy to prevent AKI in rhabdomyolysis is lacking. A recent systematic review found no level 1–3 evidence to support its use.

Mannitol also has theoretical benefits by flushing nephrotoxic agents through the tubules, it extracts fluid that has accumulated in injured muscle, and acts as a free radical scavenger. Again there was no level 1–3 evidence to support the use of mannitol in the prevention of AKI^7.

Considering the benefit achieved by alkalising the urine and forced diuresis soda bi carbonate and furosemide infusion was used in this patient. Further studies may be needed to clarify this effect.

Hence, we conclude stating the primary treatment of Acute kidney injury induced by rhabdomyolysis being vigorous fluid resuscitation with intensive urine output monitoring.

References:

1. Meijer AR, Fikkers BG, Keijzer MH, Engelen BG, Drenth JP. Serum creatine kinase as predictor of clinical course in rhabdomyolysis: a 5-year intensive care survey. Intensive Care Med 2003; 29: 1121–5
2. Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction and rhabdomyolysis. Intensive Care Med 2001; 27: 803–11.
3. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009; 361: 62–72
4. Akmal M, Bishop J, Telfer N, Norman AW, Massry SG. Hypocalcaemia and hypercalcaemia in patients with rhabdomyolysis with and without acute renal failure. J Clin Endocrinol Metab 1986; 63: 137–42
5. David WS. Myoglobinuria. Neurol Clin 2000; 18: 215–43
6. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized patients. Medicine (Baltimore) 2005; 84: 377–85
7. Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: a systematic review. Ann Pharmacother 2013; 47: 90–105)

Abbreviations :

AKI : Acute Kidney Injury

CPK : Creatinine Phospho Kinase

CK : Creatinine Kinase

BUN : Blood Urea Nitrogen

ATP : Adenosine Tri Phosphate

NS : Normal Saline

IVC : Inferior Vena Cava

Author:

Dr. Sujan Dey, Consultant Critical Care, Artemis Hospitals, Gurugram.
Dr Reshma Tewari,Director Critical Care,Artemis Hospitals,Gurugram
Dr. Urvashi Modi, Registrar Critical Care, Artemis Hospitals, Gurugram.
Dr Muneer Jan,Assoc.Consultant Critical Care,Artemis Hospitals, Gurugram
Dr. Abhishek Goyal, Registrar Medicine, Artemis Hospitals, Gurugram.

The post Acute Kidney Injury Induced by Rhabdomyolysis appeared first on CCEM Journal.

The global history of ICU care dates back to the polio epidemic in 1950s, when the specialty of critical care was born. The technique of controlled ventilation was then extended to patients with drug overdose, tetanus, and chest trauma, with resultant improvement in survival. The development of effective ventilator and improved circulatory support in post operative patients radically extended the surgical possibilities. Thereafter, ICUs then assumed the role in prevention of irreversible organ failure. The first coronary care unit in India was started in 1968 at the King Edward VII Memorial Hospital, Mumbai. Critical care units in the early 1970s, though centralized, were designed and equipped chiefly to offer intensive care to patients with acute myocardial infarction and other manifestations of ischaemic heart disease. ICUs in India have evolved from cardiac to multi-system disease care units. The newest ICU set up emerging in some advanced tertiary care hospitals is the emergency or acute care units, located in the casualty or emergency departments. These emergency intensive care units cater to first 24 hours of aggressive treatment, monitoring and stabilization of diverse emergencies, and seem to have significantly reduced the mortality¹.

Challenge:

Resource utilization and diversification in hospitals are the main challenges in the present scenario as the cost of providing and availing treatment has escalated by leaps and bounds over the last decades. Cost of treatment to patients admitted under Critical Care is often astronomical. No doubt advanced technologies, better trained manpower and evidence based practice has made treating patients a more discreet practice but along with these, the necessity for quality in medicine and medico legal compliances has made clinical activities rather defensive in nature too. Moreover with the patient’s identity being now seen also as a demanding and well informed customer has forced the clinical administrator and the clinician to have answers and alternatives for him. All these are improving the health care delivery system but at an escalation of cost which has ultimately to be borne by the care provider and reimbursed from the patient.

Health systems in every nation need innovation and improvement. But it is also important to appreciate that remedies imported from commerce have consistently yielded inferior care at inflated prices². Hence apart from our professional, moral and ethical obligations as care providers, it is imperative that we deliver quality care cost effectively^3.

Scope:

The article is an attempt to apprise busy clinicians or entrepreneurial doctors planning to set up a Critical Care Unit on certain economic and operational concepts and to provoke thoughts regarding setting up of alternate units specially a Respiratory Intensive Care Unit.

Dynamics Of ICU Care Cost:

A study⁴ published in 2008 regarding ICU costs in India stated that an estimated about 70,000 ICU beds are available including all types and across all hospitals and small time nursing homes in India that cater to five million patients requiring ICU admission every year. 80 per cent of investment will have to come from the for-profit private and charitable sector where Critical Care accounts for 20 to 30 per cent of a hospital’s budget. These numbers and demands have no doubt increased in the years.

In a for profit model, perceived financial gains may not be realized in turn forcing the organization to reengineer capital budgeting with its potential impact on service delivery. On the other hand, several government run ICUs where costs of care may exceed available funding, are noted to have limited resources, lack of infrastructure, trained intensivists and support staff. Thus routine hospital care is dependent on some form of formal or informal cost-sharing process and when the cost of intensive care is added to this burden, the clinician is faced with the dilemma of overall sustainability of the unit⁴.

Nevertheless, in appropriately selected patients, the prospects for survival in ICU are much greater than care in the general ward. It is, therefore, essential to analyze the accurate cost of intensive care and translate it appropriately for better resource allocation to benefit the critically ill⁴.

Framework For Conducting A Cost Study For Critical Care Services:

Since the last two decades, with increasing globalization, the importance of cost of care understanding has been imposed on clinicians and strategists alike. Many studies have been done in this regard and the results do not have a common finding. It varies from country to country and among the structures of national health systems.

1. Most published studies have however followed the cost block analysis system which comprised of the following⁴:
   • Cost block 1: Capital equipment
   • Cost block 2: Estates: This is defined as depreciation, maintenance and utilities necessary to maintain ICU structure.
   • Cost block 3:Non-clinical support services
   • Cost block 4: Clinical support services
   • Cost block 5: Consumables
   • Cost block 6: Manpower costs
2. Cost control measures: Any cost minimizing strategy has to be internally fashioned than being externally imposed to optimize results. At the same time quality of care will suffer if cost cutting is the sole determinant of care. Hence a balance is required. Moreover optimization of various other factors such as organization/staffing, reduction of errors/critical incidents, ongoing audits/staff training, practicing preventive intensive care/application of telemedicine etc can impact these blocks in turn bringing down the total ICU costs⁴.
3. Implementation of preventive intensive care: It is prudent to analyze ways to minimize ICU admissions or practice measures to decrease length of stay by either early optimization or preventing secondary complications⁴.
4. Minimizing errors and critical incidents: It is well proven fact that medication errors and other near misses add to the cost of care and is more common in ICU context. Solution to circumvent this include staff training, close supervision and developing a web-based anonymous reporting gateway⁴.
5. Financial and management training for ICU leaders: Most doctors have very little interest in matters pertaining to finance and accounts. This is not surprising as management and financial training is not part of medical curriculum. But it is imperative that ICU director is trained in financial decision-making. This in turn allows the intensivist to execute appropriate accounting methods, capital budgeting and resource management. Also acquiring negotiation skills will be useful in dealing with financial directors, hospital managers and other personnel funding the ICU. All these invariably translate into cost containment⁴.
6. Information technology promises to consolidate and present existing information so that clinical efficiency improves and medical errors decrease, especially for common complex conditions for which evidence-based clinical practice guidelines may be developed. Clinical informatics applications include physician order entry systems, electronic medical records with laboratory and radiology data, and computerized clinical decision support systems (CDSSs). More recently, studies of a CDSS for mechanical ventilation for patients with acute respiratory distress syndrome have shown improved patient morbidity. Whether this approach will reduce ICU costs per case (for example, by allowing the implementation of diagnostic pathways and standardizing medication use) remains to be tested⁵_.
7. Tips to remember while planning a Critical Care unit ⁶ :
   • Budget available
   • Level of ICU needed
   • Location
   • Number of Beds needed
   • Designs
   • Human Resource Development
   • Engineering and designing constraints
   • What type of Case mix the ICU team is likely to deal with and therefore help in prioritise equipment type
   • In Case of existing facility being upgraded or relocated, then the review of past mistakes
   • Patient safety and prevention of infection programme
   • Transition in case of relocation during reconstruction of the existing ICU
8. Critically assessing the need for invasive intubation and non-invasive airway support for patients before admitting in Critical Care units: Exploring the use of dedicated Respiratory Medicine Unit instead of Critical Care units specially for patients recommended for non invasive ventilation.

Rationale For Stand-Alone Respiratory Medicine Units In Hospitals:

In case of patients admitted with respiratory diseases, it is seen that in the long run either the morbidity of these patients admitted in the General Wards is increased or the patients admitted in the ICUs only for assisted ventilation support occupy beds which were required by more critical patients with other organ failure diseases. This type of arrangements led to sub-optimal use of resources as well as sub-optimal care of patients.              

1. Services to improve the care of patients with acute severe medical conditions in general and respiratory disease in particular, need to be improved. This includes access to a non-invasive ventilation service, available 24 hours per day, in all hospitals admitting patients with acute medical conditions. Patients with respiratory failure constitute a significant proportion of medical admissions and the development of appropriate services for these patients is important from both the clinical governance and the economic perspectives⁷.
2. The published report of April 2002 of the Royal College of Physicians Working Group and developed further by the NHS Modernisation Agency subgroup emanating from the expert group producing “Comprehensive Critical Care” suggested that an NIV(Non Invasive Ventilation) service should be established in each acute trust (hospital under NHS) on the grounds that selected groups of patients with acute respiratory insufficiency have been shown to benefit from this intervention. Equally importantly, it may be more suited to patients’ needs and can reduce the complication rate attributable to endotracheal intubation. The development of such a service would not only facilitate the movement of patients from level 3 to level 2 dependency, but would also afford a more palatable and dignified means of providing respiratory support to those who have little hope of being successfully weaned from mechanical ventilation owing to the chronicity and/or terminal nature of their pulmonary disease. It was also recognised that NIV should be provided in specialist centres for patients with delayed weaning and for those likely to require long term and domiciliary ventilatory support⁸.
3. Rationale For Non-Invasive Ventilation – There is now a robust evidence base for the use of non-invasive ventilation (NIV) in patients with mild (pH 7.31–7.35), moderate (pH 7.25–7.30), and severe (pH <7.25) acidotic exacerbations of chronic obstructive pulmonary disease(COPD). It is best instituted “early” before ventilatory support is definitely needed but, even when the patient appears to warrant intubation and mechanical ventilation, there is much to be gained and little to be lost by a trial of NIV. NIV has also been used in patients with hypoxaemic respiratory failure resulting from a variety of different conditions. It has been shown to be both more effective and cheaper than intubation and ventilation on the ICU and conventional treatment on general wards. It is certainly feasible outside the ICU⁹.

Criteria For Selection Of Patients For Admission To RICU:

Admission of patients to General Wards or Intermediary care units or to Intensive Care Units is done based on the following classification:

Level 0: Patients whose needs can be met through normal ward care.

Level 1: Patients at risk of deterioration in their condition and those recently relocated from higher levels of care whose needs can be met on an acute ward with additional advice and support from the critical care team.

Level 2: Patients requiring more detailed observation, including support for a single failing organ system or postoperative care, and those “stepping down” from higher levels of care.

Level 3: Patients requiring advanced respiratory support alone or basic respiratory support together with support of at least two organ systems. This level includes all complex patients requiring support for multi-organ failure.

The Respiratory Physician is usually involved with patients in Level 1–3 dependency.

In the light of these findings based on many studies carried out across the globe, it is now an accepted norm that a stand-alone and comprehensive Respiratory Medicine Unit with all facilities required for diagnostic, therapeutic and rehabilitative procedures of patients is the order of the day.

References :

1. ICU Care in India – Status and Challenges ,ME Yeolekar, S Mehta © JAPI • VOL. 56 • APRIL 2008.
2. Davis K, Schoen C, Schoenbaum SC, Doty MM, Holmgren AL, Kriss JL, et al. New York: Commonwealth Fund; 2007. Mirror, mirror on the wall: An international update on the comparative performance of American health care.
3. Indian J Crit Care Med. 2008 Apr-Jun; 12(2): 55–61. doi:  4103/0972-5229.42558PMCID: PMC2738307.
4. Cost of Intensive care: Indian perspective : Jayaram R, Ramakrishnan N. Cost of intensive care in India. Indian J Crit Care Med [serial online] 2008 [cited 2017 May 3];12:55-61. Available from: http://www.ijccm.org/text.asp?2008/12/2/55/42558.
5. The Large Cost of Critical Care: Realities and Challenges Adhikari, Neill MD, CM, FRCPC; Sibbald, William MD, FRCPC, FCCHSE Anesthesia & Analgesia: February 2003 – Volume 96 – Issue 2 – pp 311-314; doi: 10.1213/00000539-200302000-00001).
6. ICU Planning and Designing in India – Guidelines 2010 : Guidelines Committee ISCCM : Dr Narendra Rungta (Convenor); Members – Dr Deepak Govil, Dr Sheila Nainan, Dr Manish Munjal , Dr J,Divatia (President) , Dr C K Jani (Secretary).
7. Improving the care for patients with acute severe respiratory disease, M.W.Elliott, St James’s University Hospital, Beckett Street, Leeds LS9 7TF, UK:Author Affiliations, Thorax2003;58:285-288 doi:10.1136/thorax.58.4.285.
8. Pulmonary physicians, intensive care medicine and Thorax: an evolving relationship S Baudouin, Senior Lecturer in Intensive Care Medicine, Royal Victoria Infirmary, Newcastle upon Tyne, UK , T Evans,Professor of Intensive Care Medicine, Royal Brompton Hospital, London, UK :Thorax2003;58:829-832 doi:10.1136/thorax.58.10.829-a.
9. Report of Royal College of Physicians Working Group and NHS Modernisation Agency report and Executive Summary published in April 2002 –criticalcare.nhs.uk

Author:

Dr. Surajit Kumar Barua (Medical Superintendent, Narayana Superspeciality Hospital, Guwahati)

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