The statins are the most effective and best-tolerated agents for treating dyslipidemia. These drugs are competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes an early, rate-limiting step in cholesterol biosynthesis. Higher doses of the more potent statins (e.g., atorvastatin and simvastatin) also can reduce triglyceride levels caused by elevated VLDL levels. The efficacy of rosuvastatin across its dose range of 10 to 40 mg is superior to that of other statins across their dose range,although the safety is similar.

Case Report:

A 53 year old gentleman was admitted to emergency dept. with chief complaints of dizziness and vomiting for 1 day, B/L lower limb pain for 3 days. He had one episode of  syncope in the morning. He was a known case of type2 DM, Hypertension, CAD, old AWMI with TVD, mild LV dysfunction.  PTCA with stent to LAD & Left Circumflex artery was done on Oct 2013.  The patient was on cardiac medications including Rosuvastatin. Immediately in emergency  – Oxygen by Mask at 6L/min, 18 G cannula, 12 lead ECG, RBS, ABG, CBC/KFT/LFT done. Hb 8.8 g/dl, TC 10.5×10³/cumm , Platelet 150 x10³/cumm,  Ceatinine 1.50 mg/dl, BUN 42mg/dl,  Na 126mmol/l, K 7.62mmol/l , Ca 9 mg/dl, Mg 1.4 mg/dl, RBS 295 mg/dl, Total Bilirubin 0.25 mg /dl, SGOT 232 IU/l, SGPT 185 IU/l, Alk. Phosphatase 114 IU/l, Total protein 8.3 g/dl, Albumin 3.1 g/dl, Trop I 0.255ug/L, CPK 6520 IU/L, S.Myoglobin 646 ng/dl, pH 7.317,  PaCO2 16.6,  PaO2 90,  HCO3 8.3, BE -17.3. .ECG:Bradycardia with episodic VT. ECHO:Mild LV dysfunction . CXR:Normal.

The patient had ongoing bradycardia, so he was immediately shifted to cath lab and TPI (Temporary pacing) was done.He was shifted to ICU. His potassium and creatinine phosphokinase(CPK) both were very high. Hemodialysis was done. After that he was maintained on aggressive intravenous hydration and IV insulin. Provisional diagnosis was Rhabdomyolysis, which was supported by increase level of serum Myoglobin. He was on Tab Rosuvastatin 40mg once daily at bed time along with other medications.So it was Rosuvastatin induced rhabdomyolysis. His CPK decreased from 6520IU/L to 503 IU/L within 4 days.TPI was removed and patient was discharged under stable condition.

Discussion:

Rosuvastatin is a relatively new cholesterol-lowering drug ; although highly efficacious, this new statin has generated considerable controversy regarding its safety. In Canada as well as United States, many cases of rosuvastatin induced rhabdomyolysis have been reported. The incidence of rosuvastatin- induced rhabdomyolysis is not known exactly but it was presumed to be low, and similar to atorvastatin, pravastatin, and simvastatin ; Although statin induced rhabdomyolysis has been reported at rates of 1 death per 6.6million prescriptions, no deaths related to rosuvastatin induced rhabdomyolysis were reported in the literature . Heerey et al. estimated that approximately 30% of all users of statins have concomitant prescribed drugs that can inhibit statin metabolism by hepatic cytochrome P450 (CYP) system, potentially leading to rhabdomyolysis. The factors that increase the risk of rosuvastatin induced myopathy or rhabdomyolysis include increased age, renal impairment, hypothyroidism, personal or family history of hereditary muscular disorders, previous history of muscular toxicity with another statin or fibrate, consumption of grapefruit juice (more than 1 L per day), alcohol abuse, being of Chinese or Japanese descent, concomitant use of fibrates. This group of patients should be given rosuvastatin with caution. Rosuvastatin should be discontinued in patients with a creatine kinase level of more than 10 times the ULN(upper limit) with or without muscle symptoms. Liver transaminase levels should be assessed at baseline, at 12 weeks after the start of therapy or an increase in dose, and at 6-month intervals thereafter. The dosage should be reduced or therapy withdrawn if liver transaminase levels exceed 3 times the ULN. Because of the potential for rosuvastatin to increase liver transaminase levels, it should be used with caution in patients with a history of liver disease or alcohol abuse Overall, persistent elevations in liver transaminase levels are reported in 0.1-0.4% of patients taking rosuvastatin 5-40 mg. Although the exact mechanism of statin-induced rhabdomyolysis is unknown, the implicated mechanisms include the followings: first, the cholesterol synthesis blockage; which makes the skeletal muscle-cell membranes unstable due to low cholesterol content. Second, prenylated protein abnormalities causing imbalances in intracellular protein messaging. Third, coenzyme Q10 deficiency causing abnormal mitochondrial respiratory function . Rosuvastatin induced rhabdomyolysis in this patient is supported by the following: first, among the drugs used by the patient, there was no drug that known to cause rhabdomyolysis; second: myoglobin and CPK were washed out from the blood and returned towards normal within few days after discontinuation of rosuvastatin.

Conclusion:

Although highly efficacious, rosuvastatin has generated considerable controversy regarding its safety; clinicians should maintain an increased level of awareness of the potential for muscle toxicity and rhabdomyolysis, which associated with this new drug even with low dose. Accordingly, Emergent myalgias in patients under rosuvastatin necessitate immediate testing of creatine kinase and myoglobin to exclude life threatening rhabdomyolysis even with low dose.

Reference:

1. Antons KA, Williams CD, Baker SK, Phillips PS. Clinical perspectives of statin-induced rhabdomyolysis. Am. J. Med. 2006; 119: 400-9.
2. Association of Crestor (rosuvastatin) with rhabdomyolysis [Dear Health Care Professional letter]. Mississauga (ON): Astra Zeneca Canada Inc.; 2004 June 15. Available: http: //napra.ca/pdfs/advisories/ crestorhc.pdf [accessed 2008 July 28].
3. Astra Zeneca Pharmaceuticals LP. Crestor (rosuvastatin calcium) prescribing information: Wilmington, DE; 2003.
4. Brewer HB Jr. Benefit-risk assessment of rosuvastatin 10 to 40 milligrams. Am. J. Cardiol. 2003; 92: 23-29
5. Thompson PD, Clarkson P, Karas RH. Statin-associated myopathy. JAMA 2003; 289: 1681-90.

Author:

Dr. Rajib Duarah (Jr. Consultant, CCEM, Narayana Superspeciality Hospital, Guwahati)

The post Rosuvastatin Induced Rhabdomyolysis appeared first on CCEM Journal.

AKI is defined as any of the following:

1. Increase in serum creatnine by 0.3 mg/dl within 48 hours; or
2. Increase in serum creatinine to 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
3. Urine volume

Table1: Staging of AKI*

* Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32
CKD is defined as abnormalities of kidney structure or function, present for >3 months, with implications for health.

Table 2: Criteria for CKD*

* Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

It is recommended that CKD be classified based on cause, GFR category, and albuminuria category (CGA). Cause of CKD has to be assigned based on the presence or absence of systemic diseases and the location within the kidney of observed or presumed pathologic-anatomic findings.

GFR categories has to be assigned as follows:

Table 3. GFR Categories*

*Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

Albuminuria categories have to be assigned as follows:

Table 4: Albuminuria Categories*

Kidney International Supplements (2012) 2, 19–36; doi:10.1038/kisup.2011.32

Acute Kidney Injury:

The cause of AKI should be determined whenever possible. Patients should be stratified for risk of AKI according to their susceptibilities and exposures and should be managed accordingly. They should be evaluated to determine the cause of AKI, with special attention to reversible causes. Regular monitoring of these patients with measurements of serum creatinine and urine output should be done. Once AKI has resolved the patient should be re-evaluated 3 months for new onset, or worsening of pre-existing CKD.  If these patients have CKD, they should be managed as per CKD guidelines. However, if patients do not have CKD, still consider them to be at increased risk for CKD and regular follow up of these patients should be done.

Prevention and Treatment of AKI:

In the absence of hemorrhagic shock, isotonic crystalloids rather than colloids (albumin or starches) should be used for initial management for expansion of intravascular volume in patients at risk for AKI or with AKI. Vasopressors should also be added in conjunction with fluids in patients with vasomotor shock with, or at risk for AKI.⁸ In critically ill patients, insulin therapy has to be started with target plasma glucose of 110–149mg/dl.^9-11 Dietary considerations has to be given as well in the management of AKI. A total energy intake of 20–30 kcal/kg/day has to be provided in all patients with any stage of AKI. Protein intake should not be curtailed with the aim of preventing or delaying initiation of RRT. The recommended allowance is 0.8–1.0 g/kg/day of protein in noncatabolic AKI patients without need for dialysis, 1.0–1.5 g/kg/day in patients with AKI on RRT, and up to a maximum of 1.7 g/kg/day in patients on continuous renal replacement therapy (CRRT) and in hypercatabolic patients. Nutrition preferentially should be administered via the enteral route in patients with AKI.

Following is the list of Dos ans Don’ts in the management of AKI:

• Do not use diuretics to prevent AKI. Do not use diuretics to treat AKI, except in the management of volume overload.^18,19
• Do not use low-dose dopamine to prevent or treat AKI.^20,22
• Do not use fenoldopam to prevent or treat AKI. ^23,24
• Do not use atrial natriuretic peptide (ANP) to prevent or treat AKI.^25-27
• Do not use aminoglycosides for the treatment of infections unless no suitable, less nephrotoxic,therapeutic alternatives are available. In patients with normal kidney function in steady state, aminoglycosides should be administered as a single dose daily rather than as multiple-dose daily treatment regimen. Topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, can be employed when feasible and suitable.^28-34
• Do not use NAC to prevent AKI in critically ill patients with hypotension. ^35,36
• Do not use oral or i.v. NAC for prevention of postsurgical AKI. ³⁷

• A single dose of theophylline may be given in neonates with severe perinatal asphyxia, who are at high risk of AKI.
• Lipid formulations of amphotericin B rather than conventional formulations of amphotericin B should be used. In the treatment of systemic mycoses, azole antifungal agents and/or the Echinocandins should be used rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed.

Contrast-induced (CI) AKI:

In individuals who develop changes in kidney function after administration of intravascular contrast media, evaluation for CI-AKI as well as for other possible causes of AKI should be done. Assessment for the risk for CI-AKI and, in particular, screening for pre-existing impairment of kidney function should be done in all patients who are considered for a procedure that requires intravascular (i.v. or i.a.) administration of iodinated contrast medium. ⁴⁷

Dos ans Don’ts:

• Alternative imaging methods should be considered in patients at increased risk for CI-AKI. Lowest possible dose of contrast medium has to be used in patients at risk for CI-AKI. ⁴⁸
• Either iso-osmolar or low-osmolar iodinated contrast media should be used, rather than high-osmolar iodinated contrast media in patients at increased risk of CI-AKI.^49,50
• I.v. volume expansion with either isotonic sodium chloride or sodium bicarbonate solutions should always be done prior to i.v. contrast administration. Do not use oral fluids alone in patients at increased risk of CI-AKI. ⁵¹
• Oral NAC, together with i.v. isotonic crystalloids can be administered, in patients at increased risk of CI-AKI.^52,53
• Do not use theophylline to prevent CI-AKI. ^54,55
• Do not use fenoldopam to prevent CI-AKI. ^56,57
• Do not use prophylactic intermittent hemodialysis (IHD) or hemofiltration (HF) for contrast-media removal in patients at increased risk for CI-AKI.^58-60

Dialysis Interventions for Treatment of AKI:

Renal Replacement therapy (RRT) should be initiated emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist. A broader clinical outlook has to be adopted to visualize the presence of conditions that can be modified with RRT, including trends of laboratory tests, rather than single BUN and creatinine thresholds alone when making the decision to start RRT. RRT should be discontinued when it is no longer required, either because intrinsic kidney function has recovered to the point that it is adequate to meet patient needs, or because RRT is no longer consistent with the goals of care. Important to note here is that, diuretics should not be used to enhance kidney function recovery, or to reduce the duration or frequency of RRT. ⁶¹

Anticoagulation: In a patient with AKI requiring RRT, decision to use anticoagulation for RRT should be based on the assessment of the risks and benefits from anticoagulation. Anticoagulation should be used during RRT in AKI if a patient does not have an increased bleeding risk or impaired coagulation and is not already receiving systemic anticoagulation.^62,63 For such patients following is suggested:

• For anticoagulation in intermittent RRT: unfractionated or low-molecular weight

heparin.

• For anticoagulation in CRRT: regional citrate anticoagulation.
• For anticoagulation during CRRT in patients who have contraindications for citrate: either unfractionated or low-molecular-weight heparin.^64,65

RRT in patients with AKI should be initiated via an uncuffed nontunneled dialysis catheter, rather than a tunneled catheter.^62-63When choosing a vein for insertion of a dialysis catheter in patients with AKI, these preferences should be considered:

• First choice: right jugular vein;
• Second choice: femoral vein;
• Third choice: left jugular vein;
• Last choice: subclavian vein with preference for the dominant side.^66,67

Medication management and patient safety in CK:

We should take GFR into account while deciding about the drug dosing in CKD patients. Potentially nephrotoxic and renally excreted drugs should be discontinued in patients with a GFR

Dos ans Don’ts:

• Medical advice should be sought before using over-the-counter medicines or nutritional protein supplements.
• Do not use herbal remedies in people with CKD.^68,69
• Use of metformin should be reviewed in patients with GFR 30–44 ml/min/1.73 m2 (GFR category G3b) and it should be discontinued in people with GFR
• All people taking potentially nephrotoxic agents such as lithium and calcineurin inhibitors should have their GFR, electrolytes and drug levels regularly monitored.^70-77
• People with CKD should not be denied therapies for other conditions such as cancer but there should be appropriate dose adjustment of cytotoxic drugs according to knowledge of GFR.⁷⁸
• Imaging studies: The risk of acute impairment in kidney function due to contrast agent use should be assessed and balanced against the diagnostic value and the benefits involved. Following information is noteworthy:
  • Avoidance of high osmolar agents.
  • Use of lowest possible radiocontrast dose.
  • Withdrawal of potentially nephrotoxic agents before and after the procedure.
  • Adequate hydration with saline before, during, and after the procedure.
  • Measurement of GFR 48–96 hours after the procedure.^79-82
  • Gadolinium-based contrast media should not be used in people with GFR 30 ml/min/1.73 m2 (GFR categories G4-G5) who require gadolinium containing contrast media should be offered a macrocyclic chelate preparation.^83-85

Referral to specialists: referral to a specialist for kidney care for people with CKD should be advised in the following circumstances: ^86-89

• AKI or abrupt sustained fall in GFR.
• GFR
• A consistent finding of significant albuminuria (ACR >300 mg/g or AER >300 mg/24 hours.
• Progression of CKD.
• Urinary red cell casts, RBC >20 per high power field, sustained and not readily explained.
• CKD and hypertension refractory to treatment with 4 or more antihypertensive agents.
• Persistent abnormalities of serum potassium.
• Recurrent or extensive nephrolithiasis.
• Hereditary kidney disease.

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82. Heinrich MC, Haberle L, Muller V et al. Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: metaanalysis of randomized controlled trials. Radiology 2009; 250: 68–86.
83. Perazella MA. Current status of gadolinium toxicity in patients with kidney disease. Clin J Am Soc Nephrol 2009; 4: 461–469.
84. Agarwal R, Brunelli SM, Williams K et al. Gadolinium-based contrast agents and nephrogenic systemic fibrosis: a systematic review and metaanalysis. Nephrol Dial Transplant 2009; 24: 856–863.
85. American College Radiology Guidelines. Manual on Contrast Media Version 8. http://www.acr.org/B/media/ACR/Documents/PDF/Quality-Safety/Resources/Contrast%20Manual/Nephrogenic%20Systemic%20Fibrosis.pdf. Accessed October 12, 2012.
86. KDIGO AKI Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney inter., Suppl. 2012; 2: 1–138.
87. KDIGO GN Work Group. KDIGO clinical practice guideline for glomerulonephritis. Kidney inter., Suppl. 2012; 2: 139–274.
88. KDIGO CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease- Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl 2009; 76(Suppl 113): S1–130.
89. KDIGO BP Work Group. KDIGO clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney inter.,Suppl. 2012; 2: 337–414.

Author:

Dr. Shashank Gupta (Consultant Nephrologist & Renal Transplant Physician, Narayana Superspeciality Hospital, Guwahati)

The post Do’s And Don’t in Nephrology appeared first on CCEM Journal.

Intractable status epilepticus not responding to conventional pharmacotherapy after residual tumor debridement and cranioplasty. Such refractory status epilepticus has led to the use of anesthetic drugs. Tumor location and histology influences the risk for refractory seizure. Clinically tumor related seizures manifest as simple or complex partial seizures with or without secondary generalization and in more than 50% cases are pharmacoresistant. When uncontrolled, tumor related epilepsy affects patient’s quality of life, causes cognitive deterioration and may result in significant morbidity. Tumors involving frontal temporal and parietal lobes are more commonly associated with seizures than an occipital lesion. The frequency of seizure differs widely according to tumor type. Glio-neuronal tumors such as gangliogliomas and disembryoplastic neuroepithelial tumor are typically associated with chronic pharmaco resistant epilepsy in up to 90-100%.

Case Study:

A 38 year old male admitted in hospital for cranioplasty with p/h/o craniotomy for gangloglioma. Patient was chronic alcoholic and  had h/o of seizure disorder since 2012. Earlier he underwent  craniotomy in march 2016. He was on tablet levetiracetam 500 mg BD. Sample biopsy of lesion was suggestive of active gliotic lesion. Its CT finding showed temporal gliotic area with central necrosis and hemorrhagic in nature. Patient underwent cranioplasty on 14/12/16. Two days later a witness GTCS was reported. Initially infusion medazolam was started @ 2mg/kg/hr. but focal partial seizures continued. Other antiepileptic drugssuch as T. Levetiracetam 750 mg, T.Sodium valproate 500mgT Frisium 10 mg, and T Librium was added. The regimen was continued for next 2 days, but there was no reduction in frequency of seizures. Thereafter higher anesthetic drugs were introduced. Initially treatment started with infusion propofol @ 3mg/kg followed by inj Lorazepam 4mg IM 6 hrly. Infusion continued for next 48 hours. No relief achieved and partial focal seizure continued. Infusion propofol was stopped and Thiopental was added to the regimen @ 3mg/kg/hr for next 24 hours. Reduction in seizure frequency was observed. Infusion Dopamine was added to maintain hemodynamic stability. Post SOL resection was done on 21/12/16. There after thiopentone infusion was continued. Total reduction of seizures were observed. Slowly Thiopentone was tapered and stopped on 26/12/16. Infusion Medazolam was started as maintenance. No event of seizure was reported thereafter. Patient was extubated on 31/12/16 and was put on oral antiepileptic. With  inj. phenobarbitone 100mg BD and inj.Levetiracetam 1gm TDS.

Discussion :

Thiopental is an intravenous anesthetic agent used for refractory SE. it is more commonly used in Europe for treating status epilepticus, is loaded at 2 to 4 mg/kg and then infused at 3 to 5 mg/kg/h. The half-life is 3 to 11 hours at serum levels < 30 mg/L, but is significantly prolonged up to 60 hours at higher serum concentrations. Hypotension appears to be most profound with barbiturate therapy. Once seizures have been controlled for 12-24 hours, continuous intravenous therapy should be gradually tapered off if the drug being administered is midazolam or propofol. Gradual tapering is probably not necessary with pentobarbital or thiopental sodium. During withdrawal of anaesthetic therapy, intravenous phenytoin/fosphenytoin or valproate should be continued (these agents having been administered during earlier phases of GCSE) to ensure an adequate baseline of antiepileptic medication so as to prevent the recurrence of status epilepticus. These agents have several inhibitory effects on lymphocyte and leukocyte functions causing increased infection rates in patients treated with barbiturate coma. Routine surveillance cultures of blood, urine, and sputum are recommended for patients on long-term therapy.

Conclusion :

We conclude that tightly controlled by serum levels and carefully monitored for therapeutic efficiency, initiating and tapering of Thiopentone infusion in the ICU setting with mechanical ventilation and hemodynamic monitoring will allow the physician to establish the therapeutic serum levels of anesthetic agents. It will help to reduce the relapse rate and to avoid the mortality and long term morbidity associated with this life threatening medical emergency.

References:

1. https://www.ncbi.nlm.nih.gov/pubmed/16142991
2. SEIZURES AND STATUS EPILEPTICUS IN THE ICU/ZIAI, KAPLAN
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4099906/
4. http://www.bcmj.org/articles/guideline-management-convulsive-status-epilepticus-infants-and-children
5. http://www.anaesthesiauk.com/documents/EpilepsyandAnaesthesia_final.pdf

Author:

Dr. Swapnil Thorat (Fellow, CCEM, Narayana Superspeciality Hospital, Guwahati)

The post Intractable seizures and role of Thiopentone infusion in post craniotomy for active gliotic lesion appeared first on CCEM Journal.

Estimated deaths due to snake bites are more than 46,000 annually in India. Ninety-seven percent bites occur in rural areas. Data on snake bite from north-east india is negligible. This study describes 3 years profile of snake bite patients from September 2014 to October 2016 at Narayana Superspeciality Hospital, Guwahati.

Introduction:

Seventy five patients were enrolled in the study. The peak incidence (64%) of snake bite occurred in June to September period ( in the monsoon season). 84 % of the bites  were non poisonous in nature. In majority of the cases (65.33%) bite mark was present. Majority of the bites were in lower limbs (61.33%) followed by upper limbs (28%). Majority (46.66%) of the patients presented within 1 to 2 hours to the hospital, overall 94.66% of the patients presented within 5 hours of alleged snake bite. 22.66% of the patients had received some form of nonmedical treatment locally before presenting to this hospital. 12% received Anti snake venom at this hospital. No form of ASV associated complication was documented. There was no in hospital mortality.

Context:

Snake bite is a major public health problem in India. According to the “million death” study, the estimated annual death due to snake bite in the year 2001–2003 ranged from 40,900 to 50,900 with the mortality rate being higher in the rural areas (4.8–6.0/100,000). Bihar had the third highest annual snake bite related deaths (4500 annually). At the same time, the Indian Government’s official figure shows national death rate below 2000 deaths/year. Thus, there is remarkable under-reporting of the snake bite related deaths.[1] There is a paucity of data on snake bite and related events, the cost of care in the snake bite management despite being a major public health problem in India.

Of the four medically important poisonous families of snakes (Elapidae, Viperidae, Atractaspidinae, Colubridae), the Viperidae (viper) and the Elapidae (Cobra and common Krait) remain the most common species of snakes responsible for most of the envenomation in Indian subcontinent

Aim:

We conducted this retrospective descriptive study in a tertiary care hospital in Kamrup  district of Assam to describe the various epidemiological, clinical features, outcome related to snake bite over a period from 2014 to 2016.

Population:

All the patients (irrespective of age) presented with the alleged history of any bites between the year 2014 to 2016 were screened from the emergency register. The patients who received the discharge diagnosis of “snake bite” based on the documentation of fang marks at the alleged site of envenomation with or without oozing of the blood as confirmed by the attending physician were enrolled in the study. The patients not fulfilling the above criteria or those with confirmed bite by any other organism (e.g., lizard) were excluded.

Materiel 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 bites between the year 2014 to 2016 were screened from the emergency register.

Results:

Epidemiological profile:

Demographic details and trend analysis : from September 2014 to October 2016, a total of seventy five patients were enrolled in this study. 60% of the patients were males (45) and the rest female (30).

Seasonal  variation of the snake envenomation cases over the 3-years period: the peak incidence of the snake bite occurred around the month of June to September which corresponds to monsoon season.

District-wise distribution and delay in presentation of the cases

Narayana Superspeciality Hospital, Guwahati is situated in the district of Kamrup of Assam. Of the total patients 55(73.33%) of the patients were from kamrup district and the rest from adjacent districts.

Clinical Profile:

Site of bite : The distribution of site of bite was was available for 67 patients. The most common site being lower limbs (61.33%) followed by upper limbs (21%). The bite in foot and leg was primarily due to accidental encounter with the snake during farming.

Anti-snake venom treatment: The data on doses of ASV were available for 9 patients. 5 patients received < 5 vials of ASV, while 4 patients 5-10 vials.

Outcome : Of the 75 patients 9 patients (12%) were treated with ASV. None expired. No case of anaphylaxis to ASV was noted among the recipients.

Discussion:

Snake bite is a major public health hazard and neglected tropical disease in India. Most of the snake bite cases occur in the rural areas and in the monsoon months from June to September. The estimated annual death due to snake bite in India is nearly 50,000 persons. The data on the true burden of the disease, role of polyvalent ASV, incident of ASV anaphylaxis, and treatment outcome from rural set up are scarce.  As per the national mortality survey in 2001–2003, approximately 4,500 deaths occur annually in the state of Bihar and ranks third among snake bite related deaths in India. Despite this, there has been a paucity of data from this region.

This is the first large descriptive study on the clinico-epidemiological profile and the treatment outcome of the snake bite cases from a tertiary care center of assam, India.  On analyzing the seasonal variability of the snake bite cases, we found that more than 64% of the cases occur during the monsoon months (june to September). The interesting outcome of this study was that most of the bite were of non poisonous snakes. In case of poisonous bites the severity of poisoning was mild. There was no major anaphylactic reaction to Anti snake venom. The outcome of all the patients was good. Presentation to a medical centre was early. The most common site of the bites were in lower limbs .

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

References:

1. Mohapatra B, Warrell DA, Suraweera W, Bhatia P, Dhingra N, Jotkar RM, et al. Snakebite mortality in India: A nationally representative mortality survey.PLoS Negl Trop Dis. 2011;5:e1018. [PMC free article][PubMed]
2. Majumder D, Sinha A, Bhattacharya SK, Ram R, Dasgupta U, Ram A. Epidemiological profile of snake bite in south 24 Parganas district of West Bengal with focus on underreporting of snake bite deaths.Indian J Public Health. 2014;58:17–21. [PubMed]
3. Brunda G, Sashidhar RB. Epidemiological profile of snake-bite cases from Andhra Pradesh using immunoanalytical approach.Indian J Med Res. 2007;125:661–8. [PubMed]
4. Kumar MR, Veeraprasad M, Babu PR, Kumar SS, Subrahmanyam BV, Rammohan P, et al. A retrospective review of snake bite victims admitted in a tertiary level teaching institute.Ann Afr Med. 2014;13:76–80. [PubMed]
5. Halesha B.R., Harshavardhan L, Lokesh A.J, Channaveerappa P.K., Venkatesh K.B. A study on the clinico-epidemiological profile and the outcome of snake bite victims in a tertiary care centre in southern India.J Clin Diagn Res. 2013;7:122–6. [PMC free article] [PubMed]
6. Bawaskar HS, Bawaskar PH, Punde DP, Inamdar MK, Dongare RB, Bhoite RR. Profile of snakebite envenoming in rural Maharashtra, India.J Assoc Physicians India. 2008;56:88–95. [PubMed]
7. Raina S, Raina S, Kaul R, Chander V, Jaryal A. Snakebite profile from a medical college in rural setting in the hills of Himachal Pradesh, India.Indian J Crit Care Med. 2014;18:134–8. [PMC free article] [PubMed]
8. Bhardwaj A, Sokhey J. Snake bites in the hills of north India.Natl Med J India. 1998;11:264–5. [PubMed]
9. Alirol E, Sharma SK, Bawaskar HS, Kuch U, Chappuis F. Snake bite in South Asia: A review.PLoS Negl Trop Dis. 2010;4:e603. [PMC free article] [PubMed]
10. WHO. Snakebite.WHO. [Last cited on 2014 Nov 02]. Available from: http://www.who.int/neglected_diseases/diseases/snakebites/en/
11. Punde DP. Management of snake-bite in rural Maharashtra: A 10-year experience.Natl Med J India. 2005;18:71–5. [PubMed]
12. Chaudhari TS, Patil TB, Paithankar MM, Gulhane RV, Patil MB. Predictors of mortality in patients of poisonous snake bite: Experience from a tertiary care hospital in central India.Int J Crit Illn Inj Sci. 2014;4:101–7. [PMC free article] [PubMed]
13. Vijeth SR, Dutta TK, Shahapurkar J, Sahai A. Dose and frequency of anti-snake venom injection in treatment ofEchis carinatus (saw-scaled viper) bite. J Assoc Physicians India. 2000;48:187–91. [PubMed]
14. Paul V, Pratibha S, Prahlad KA, Earali J, Francis S, Lewis F. High-dose anti-snake venom versus low-dose anti-snake venom in the treatment of poisonous snake bites – A critical study.J Assoc Physicians India. 2004;52:14–7. [PubMed]
15. Cherian AM, Girish TS, Jagannati M, Lakshmi M. High or low – A trial of low dose anti snake venom in the treatment of poisonous snakebites.J Assoc Physicians India. 2013;61:387–9, 396. [PubMed]

Author:

Dr. Akash Baruah (Fellow, CCEM, Narayana Superspeciality Hospital, Guwahati)

The post A study on clinico-epidemiological profile and the outcome of snake bite victims in a tertiary care centre appeared first on CCEM Journal.

Hanging is one of the leading cause of death in the world accounting for 1 million death annually¹. In India hanging is the 2^nd most common method of suicide after poisoning².

Hanging is a violent death produced by suspending the body with ligature around the neck, the constricting force being the weight of the body or a part of body. Hanging can be classified as various types as typical or atypical according to knot position, complete or partial on the basis of degree of suspension, suicidal, accidental or homicidal on the basis of manner  of death and others³. Death usually occurs due to cervical injury as occurs commonly in judicial hanging ⁴ or cerebral hypoxia or cardiac arrest (due to vagal stimulation)^5,6 or other complication like aspiration, post obstructive pulmonary oedema, ARDS, seizure^7,8,9,10. Although it is a common mode of suicide in India, very less data is available on its epidemiology. Here we share our experience of managing 4 cases of hanging over a period of one year.

Case Study:

CASE 1

A 14 year old girl presented to ER with alleged history of suicidal hanging followed by loss of consciousness. On presentation she was unconscious (GCS of 6) and her vitals were pulse 160/min., BP of 80/50 mm of Hg, respiratory rate of 34/min and spo2 70% with 5L O2 with bilateral crepts on auscultation. Ligature mark was present around the neck. Following ABC protocol she was immediately intubated to secure airway. Patient was then shifted to ICU and put on mechanical ventilation (VCV-AC) mode. An initial fluid challenge of 1L was given over 1 hour. An indwelling catheter and ryles tube was introduced. Central venous access was secured. Routine blood investigations, ABG, chest X-ray, X-ray cervical spine and CT brain were advised. She was started on vasopressor agents in view of persistent hypotension despite adequate fluid resuscitation. Her chest X-ray showed bilateral diffuse opacities and in view of poor oxygenation in successive ABGs and inability to maintain saturation, ARDS NET protocol was used and lung recruitment measures were started. Patient was sedated with morphine infusion with interruption of brief periods. She was started on antibiotics according to hospital antibiogram as she was spiking fever on 2^nd day with increase of TC. All of cultures were reported negative. A neurology opinion was also taken. Her CT brain and X-ray cervical spine were unremarkable. She was also given intermittent boluses of diuretics when her hemodynamics permitted. Other supportive care like heparin was used as DVT prophylaxis, pantoprazole as ulcer prophylaxis and her sugars were targeted between 140 -180mg/dl. Gradually patient’s hemodynamic status improved by 3^rd day and vasopressor were tapered off. Her oxygenation status also improved. She was gradually weaned of ventilator and extubated by 5^th day and shifted out of ICU on 6^th day. FOCUS ON: She was treated as a case of post obstructive pulmonary oedema and responded promptly to appropriate therapy which is aimed at reversing hypoxia and removing excess fluid from lung interstitium

CASE 2

A 45 year old male presented to ER with alleged history of suicidal hanging within 2 hours. Duration of hanging was not known. He had history of depression and not talking to anyone for last 6 months. During presentation his GCS was E1V2M5 with pulse of 51/min, BP of 90/60 mm of Hg and respiratory rate of 30/min with stridor but was able to maintain a saturation of 100% with 5L O₂. Cervical collar was used for precaution and patient was intubated in view of border line GCS and shifted to ICU for further management. He was managed conservatively with antibiotics, nebulisation, steroids and mechanical ventilation. His CT  brain and cervical X-ray was unremarkable. His sensorium improved and was extubated on 3^rd day, shifted out of ICU on day 4rth and discharged on 5^th day with advice of psychiatric consultation.

CASE 3

A 35 year old alcoholic male with alleged history of suicidal hanging where hanging time was 2-3 minute and was rescued by his relatives. During presentation he had ligature mark around his neck, had stridor with GCS of E2V2M5, pulse of 120/min. BP of 150/10 mm of Hg. He was intubated in ER and shifted to ICU for further management. He was conservatively managed with nebulisation, antibiotics, steroid and mechanical ventilation. He weaned off ventilator on 3^rd day. During stay he had alcohol withdrawal which was managed accordingly. He discharged on 4rth day with advice for psychiatric opinion.

CASE 4

A 15 year old girl with alleged history of hanging presented to ER after 4 and ½ hours of hanging and the duration of hanging was not known. At presentation she was unconscious with GCS of 3, pulse of 163/min. BP of 110/70 mm of Hg and respiratory rate of 40/min. with SPO2 of 78% at room air. After securing airway in ER she was shifted to ICU for further management. During ICU stay she had convulsion and her neurological status dint improve. Neurology opinion was sought and MRI was done which showed hypoxic changes. She was being managed conservatively with mechanical ventilation, antibiotic, steroid anticonvulsant and other supportive measures like sugar control, DVT prophylaxis and ulcer prophylaxis. She was planned for tracheostomy. Her outcome was not known as she was lost to follow up.

Discussion:

The term near hanging refers to a patient who initially survives the attempt of hanging and in spite of high associated fatality rate survival is possible¹¹ with aggressive measurement which include establishment of safe airway, treating pulmonary manifestation and complication, maintaining hemodynamic stability and preventing any other secondary organ injury, lowering ICP and ensuring adequate cerebral oxygenation.

In case of suicidal hanging there is minimal drop which leads to compression of neck soft tissue leading to jugular venous obstruction resulting in loss of consciousness. This leads to loss of muscle tone allowing for further tightening of ligature around the neck and subsequent carotid artery obstruction with or without airway closure^{12, 13, 14}, whereas in judicial hanging body drops from a height equal to or more than persons height which causes forced hyperextension of head with cervical spine fracture and spinal cord injury leading to death^{12, 13}. Spinal injury although uncommon, but occurs in near hanging¹⁵. Occurrence of cervical spine fracture is influenced by age, suspension time, drop from a height^{12, 16, 17}. None of our cases had cervical injury and was ruled out by CT imaging after initial stabilisation of patients.

Regarding prognostic markers some study group concluded that a SBP <90, GCS <8 and hypoxic injury in CT brain predicted a poor prognosis¹² while other groups highlighted profoundly depressed GCS or cardio pulmonary arrest as poor prognostic markers. In our patients 2 had profoundly depressed GCS of which one had hypoxic injuries in MRI and in other patient outcome was good. The other 2 patients with borderline GCS improved well. Other prognostic markers long hanging time¹⁸ and drop height >body height¹⁹ could not be assessed in our cases. Regarding respiratory complication none of the patient showed any finding of aspiration though it is one common complication, where as one patient developed Post Obstructive Pulmonary Edema and was managed by positive pressure ventilation with diuretics and judicial use of IVF and could be discharged of hospital by 6^th day. None of the patient had retinal bleed. Only one patient had seizure( who showed hypoxic damage in CT brain). There is high incidence of both the above complication, but of little prognostic value.

FOCUS ON: In our case management was aimed at

• Stabilisation of neck and radiological clearance.
• Securing airway with endotracheal tube and positive pressure ventilation.
• Judicial use of IVF to maintain hydration and to avoid overload.
• Control of ICP and cerebral edema.
• Prevention and management of respiratory complications.
• Other supportive measure like DVT prophylaxis, ulcer prophylaxis and good sugar control.

References:

1. Mohanty S, Sagu H, Mohanty MK, Patnaik M. Suicide in India: A four year retrospective study. J Forensic Leg Med 2007; 14(2):185-1891.
2. David Gunnell, Olive Bennewith, Keith Hawton, Sue Simkin and Nav Kapur. The epidemiology and prevention of suicide by hanging: a systematic review. International Journal of Epidemiology 2005; 34(2):433-442.
3. Vij K (2001) Textbook of Forensic Medicine, Principles and Practice. 1st edition, New Delhi: Churchill Livingstone Pvt, 62.
4. Nithin MD*, Manjulatha B, Pramod Kumar GN and Sasidharan Sameer. Delayed death in hanging.
5. Nageshkumar G Rao (2010) Forensic Medicine & Toxicology. 2nd edition Jaypee Brothers Medical Publishers, 179, 195.
6. Dimaio VI , Dimaio D (2001) Forensic Pathology, 2nd edition, CRC Press, USA, 245-257.
7. Nair S, Jacob J, Aaron S, Thomas M, Joseph M, et al. (2009) Pulmonary distress following attempted suicidal hanging. Indian J Med Sci 63:53-57.
8. Fischman CM, Goldsmith MS, Gardner LB (1977) Suicidal hanging an association with the adult respiratory distress syndrome. Chest 71: 225–227.
9. Digeronimo RJ, Mayes TC (1994) Near-hanging injury in childhood: A literature review and report of three cases. Pediatr Emerg Care 10: 150-156.
10. Hoff BH (1978) Multiple organ failure after near-hanging: A case report. Crit Care Med 6: 366-369.
11. Salim A, Martin M, Sangthong B. Near-hanging injuries: a 10-year experience. Injury 2006;37:435–9.
12. Newton K. Neck. In: Marx J, Hockberger R, Walls R, eds. Rosen’s Emergency Medicine_Concepts and Clinical Practice. 7th edn. Philadelphia: Mosby; 2010:377–86.
13. Martin MJ, Weng J, Demetriades D. Patterns of injury and functional outcome after hanging: analysis of the National Trauma Data Bank. Am J Surg 2005;190:838–4315.
14. Adams N. Near hanging. Emerg Med 1999;11:17—21.
15. Penney DJ, Stewart AHL, Parr MJA. Prognostic outcome indicators following hanging injuries. Resuscitation
    2002;54:27—9.
16. Morilid I. Fractures of neck structures in suicidal hanging. Med Sci Law 1996;36:80–4.
17. Matsuyama T, Okuchi K, Seki T, Murao Y. Prognostic factors in hanging injuries. Am J Emerg Med 2004;22:207—10.
18. Davidson JA. Presentation of near-hanging to an emergency department in the Northern Territory. Emerg Med. 2003;15:28–31

Author:

Dr. Suman Nandi (Jr. Consultant, CCEM, Narayana Superspeciality Hospital, Guwahati)

The post Hanging 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)

The post A Brief Overview For Clinician’s Orientation To ICU And Alternative Planning appeared first on CCEM Journal.

There are studies emphasizing the importance of arterial blood lactate level on outcome, specifically mortality in patients with circulatory shock, cardiac arrest, trauma, sepsis, septic shock, ards, pulmonary embolism and cardiovascular outcome, but its prognostic significance in mixed icu population is not well defined.

Objective:

To examine whether value of arterial blood lactate level on admission to a general intensive care unit with mixed populations of septic and non septic patients can indicate prognosis.The primary outcome measured is 28 day mortality.

Design:

Prospective Observational study.

Setting: General adult intensive care unit in a tertiary care teaching hospital.

Interventions: Arterial blood samples were obtained on admission to the intensive care unit.

Patients: 224 consecutive patients admitted to the intensive care unit. Patients are split into two groups namely septic and non-septic from final diagnosis.

Measurements and results:

For statistical calculation, we used Stata/SE 11 software. Out of Total 120 septic patients 25 patients lost to follow up and Out of 104 non-septic patients 19 lost to follow up, so excluded from the study for 28 days mortality. In all patients whose initial arterial blood lactate levels were >1.9, the unadjusted and adjusted odds ratios are 3.64 (2.00 – 6.62) and 3.30 (1.66-6.57) with 95% CI and p value of 0.001. Inseptic patients the area under ROC curve is 0.7794 and the same for non-septic patients is 0.8657. The area under ROC curve for all patients (total 180) is 0.7447.

Discussion:

In a study by Wong DT(Crit care med,1995),Apache II ROC curve is 0.860 for prediction of hospital mortality.More recently PROWESS study(Richards G, J intensive care med, 2011) the patients with community acquired pneumonia in placebo arm, the ROC for Apache score of  ≥ 25 was 0.64 for 28 day mortality.  Our study ROC Curve for mixed ICU population is 0.7447 for prediction of mortality at 28 day. It is a very easy accessible and relatively cheap measure. Its ability favorably compares to apache II.

ALL ICU PATIENT MORTALITY ROC

ROC SEPTIC PATIENTS = 0.779

ROC NON SEPTIC PATIENTS = 0.8657

Conclusion:

Admission arterial blood lactate level can be used to predict outcome in patients admitted to the intensive care unit. This variable may be utilized to identify patients who have a high risk for mortality and thus who should be admitted to the intensive care unit. The limitation of the study is that it is a single centered study.

Author:

1. Dr. Apurba Kumar Borah (Consultant & HOD, CCEM, Narayana Superspeciality Hospital, Guwahati)
2. Dr. Vikram Khatri (Director CCEM & Peri-operative Services, Moolchand Medcity, New Delhi)

The post The Prognostic value of Admission Arterial Blood Lactate Level in Mixed ICU Population appeared first on CCEM Journal.

The outcome of  ICU patients  is directly related to the clinical nursing attention they receive during the severe illness. So to achieve that  we designed a unique portable cart able to be stocked with commonly used patient care equipments. We find that this new cart system can significantly increase the clinical time by the nurse with each assigned patient which results significant improved outcome.

Introduction:

The outcome of patients admitted in ICU is closely related to the nursing attention they receive during the severe illness. There are a number of obstacles to a Intensive care nurse tasked to provide patient care. Obstacles identified include delay in getting medications, stocking issues in patient rooms, insufficient workspace for completing paperwork, seeking for supplies or patients’ charts and misplaced equipment. ¹ There are negative impacts of these obstacles on patient safety and quality of healthcare delivered as perceived by the nurses.² Therefore, optimizing nurse ergonomics should results in more clinical time, short response time and fewer errors and complications.

Objectives:

To determine if the introduction of a bedside cart system will maximize the clinical time spent by nurses with their respective patients, save time to completion of tasks and result in a better transfer of care. Further to assess subjective comfort/ease in the nurses at baseline and after 6 months of implementation.

Methods and Materials:

We designed a unique portable bedside cart able to be stocked with commonly used patient care equipment. Preliminary stages of design had to figure in the designated spaces and holders for drugs, fluids, consumables, gloves, hand hygiene and patient related charts. Fig 1. Ergonomic designing required calculating the average height of the nursing staff, depth of the cabinets and locations of the drawers. Transportation and maneuverability was addresses with designing in of large wheel. Safety and regulatory concerns were solved by providing for locked cabinets. There are three drawers with one has a facility for locking which is the largest of all and this locked drawer is used to keep all articles locked when the cart is not in use and kept stand by. Fig: 2. Such a cart is designed pre-packed to be used at immediate notice. Fig: 3.

We then formulated three mock-standardized drills namely new patient admission, patient care and nursing handover. No human subjects were involved. A Patient Dummy was used. New patient admission drill, included starting of oxygen, placing patient on monitor, IV line placement and starting of IV fluids.  Providing routine care, mock drill included sample collection, administration of antibiotics and initiation time of back care and washing. Nursing handover drill included handing over of files and inventory.

Three nurses were randomly chosen and assigned to different mock drills. Each nurse had to perform the tasks with the bedside cart or the traditional centralized supply cabinet model. All the tasks were timed. Time keeping was done with stopwatch in a cellular phone.

Respective nurses were then asked to grade their individual tasks subjectively by means of a Questionnaire with 0 to 10 scoring. We calculated mean scores of all the three mock drills subjective assessments. The questionnaire was simply a lists of tasks routinely carried out by nurses.

No subjective element was present therefore external validation was skipped.

At Six-month post implementation of the cart system we polled all the nurses with six-month experience each in the cart vs non-cart system.

Figure 1:  Preliminary Schematic Design

Figure 2: Inventory List for the cart

Figure 3: Ready to use cart

Table1: Result of Mock Drill

Table: 2

Post Drill Mean Scores of Subjective Assessment (0= Most Easy/Minimal Effort and 10=Most Difficult/Maximal Effort to accomplish task)

Table: 3

Mean Score Subjective assessment of nurses at six month of use

(0= Most Easy/Minimal Effort and 10=Most Difficult/Maximal Effort to accomplish task)

Results:

Results show a significant improvement in time to complete each task.

10s Vs 40s to start oxygen, 40s Vs 70s to start monitor, 50s Vs 2 min 40s for starting IV fluid, 60s Vs 2 min for blood sample collection, 70s Vs 100s for administration of antibiotic, 7s Vs 30s for initiation of back care and back care/washing, 2 min 25s Vs 3 min for file handover and 25s Vs 30s for inventory handover. (Table 1). An average reduction of about 4 to 5 point reduction in work effort was noticed. (Table 2).  A subsequent survey of nurses at six-month reveal that the perception of effort reduction to complete tasks persists after long use. (Table: 3)

Discussion:

Task completion has to be efficient and multitasking is essential in the complex environment of ICU. Ease of task would result in higher fidelity care and translate in better patient outcomes and staff satisfaction.

Patients should get the care he or she deserves in a timely and in a proper manner, which is directly related to the clinical time spent by the nurse.¹². There are lots of performance obstacles of intensive care nurse, who is the final caregiver in the process ¹. The compliance to glycemic control, agitation prevention, nutrition, infection control, prevention of medication errors are directly related to quality of nursing care the patient receives. Further, patient safety is directly attributed to their working condition.¹²

Numerous studies have demonstrated benefit of higher nurse patient ratios in hospitals.⁴ Trained nursing workforce in ICU is also a scarcity in India and as evident from abroad there is a consequence to it.⁵ But, there is cost to increasing workforce, which has to borne by the patients. India is a poor country especially in respect of the healthcare economics. Therefore achieving efficiency should be high priority. Concepts like Lean and 5S have been implemented in healthcare with success.^6,7,8,9. Thinking from human angle is mandatory in organizing new workplaces. There are a few successful examples that a devolution of power and combining LEAN, 5S and human factors have led to safety and better delivery of care.^10,11 Our focus was to design the bedside cart in an attempt to maximize the time spent by a critical care nurse with his or her respective patient. As we noticed there was substantial improvement in time taken for each assigned task for completion. In addition, the ease task completion was also improved. Encouraged by the results and persistent nurse satisfaction we have implemented this system across our institution.

Limitations of our study were that is it is a single center study, subjective assessment is involved.

Conclusions:

We noticed that after introduction of this new cart system in our ICU, the clinical time spent by the nurse with each assigned patient impressively increased. This has resulted in increased early detection of bad physiology, timely and proper medication, less medication errors and significant improved outcome.

Author:

1. Dr. Apurba Kumar Borah (Consultant & HOD, CCEM, Narayana Superspeciality Hospital, Guwahati)
2. Dr. Vikram Khatri (Director, CCEM & Peri-operative Services, Moolchand Medcity, New Delhi)
3. Dr. Sardar Hyder Ali Khan (Jr. Consultant, CCEM, Moolchand Medcity, New Delhi)
4. Dr. KRISHNA C. K. (Jr. Consultant, CCEM, Moolchand Medcity, New Delhi)

The post Bedside Cart System And Its Effects On Work Dynamics of Critical Care Nurses appeared first on CCEM Journal.

Advantages of Point of care testing:

1. Reduced TAT
2. Improved patient management
3. Reduction in the administrative work associated with test requesting
4. Reduction of the risk of a disconnection before the process of testing and clinical decision making.

Factors that need to be considered in the implementation a POCT service:

1. Establishing need
2. Establishing a POCT testing policy & accountability
3. Training and certification of operators
4. Establishing QC , quality assurance & audit policy.
5. Establishing documentation.

The key points in maintenance and inventory control are to adhere to the recommend storage condition, be aware of the shelf life of the consumables, ensure that stocks are released in time. Issues that usually require particular vigilance include expiration date, bio-contamination, electrical safety & maintenance of optics.

Classically quantitative internal QC involve the analysis a sample for which the analyte concentration is known and the mean and range of result quoted for the method used. QC testing strategy that may be used — analyze a minimum of one QC sample per run during each shift. If testing is infrequent then another approach would be to analyse a QC sample whenever there is a change to the testing system, such as a different batch of testing material or a different operator.

There are hardly any specific literature based on Randomised control trial(RCT) and cost effectiveness study . Although POCT has the potential to provide beneficial patient out come, further study may be required, especially for defining its real utility on clinical decision making.

Author:

Dr. Rizwn Athar (Consultant, Pathologist, Narayana Superspeciallity hospital, Guwahati)

The post Point of Care Testing (POCT):Where are we? appeared first on CCEM Journal.

Catheter associated urinary tract infection is an important cause of mortality and morbidity. Its incidence in India as per available study is 22.22%(Col Shivinder Singh et al, medical journal armed forces India,2013) among all nosocomial infections. Its burden on healthcare is immense. With changing time and increasing no of hospital beds worldwide, which subsequently increasing the no of patients being catheterized,it’s now more relevant to address this menace with new techniques.

Material and method:

All patients with a urinary catheter were enrolled in the study from 15^th January’2017 till 30^th of April ’2017 and data’s were collected.  Apart from maintaining the standard CAUTI bundle suggested by CDC, we have introduced one simple intervention in our cauti prevention bundle. That is application of 1.0% chlorhexidine gel every 6 hourly. The gel is applied over the outer surface of urinary catheter starting from meatal part proximally to the catheter fixation part distally to the urobag. The calculation of cauti is done using the following formula.

Number of cauti in the month

CAUTI Rate :       ——————————————-  x 1000

Number of Catheter days

Starting with a CAUTI rate of 7.02% , the rate declined to 1.01% within a month and sustained at 4.22% and 3.3% in the subsequent months.

Discussion:

Significant serious efforts are being made world wide to decrease this nosocomial problem. There are good guidelines made available by various bodies , especially CDC in curbing this problem. New research are still going on in this area. There are studies which shows effectiveness of antimicrobial urinary catheters (Johnson JR, Systemetic review,Ann Intem Med,2006) but these are costly. One systemic review concludes that this of course decreases the catheter associated bacteriuria and funguria (Drekonja DM,Expert review med devices,2008) but there is variable evidences and future studies are recommended. In our study we emphasized on using a very simple and cheap method and the results are encouraging. There is significant drop in the incidence of CAUTI as illustrated in the figures.

Conclusion:

We therefore conclude that application of chlorhexidine gel(1%) on urinary catheter has a positive impact on decreasing CAUTI rate. We are currently continuing the method and in future will come up with more elaborate analysis.

Author:

1. Dr. Apurba Kumar Borah (Consultant & HOD, CCEM, Narayana Superspeciality Hospital, Guwahati)
2. Ms Shaini Roel (Infection Control Nurse, Narayana Superspeciality Hospital, Guwahati)

The post Application of 1.0% Chlorhexidine gel and its effect on Catheter associated urinary tract infection (CAUTI) in a tertiary care hospital in north east India appeared first on CCEM Journal.