Fat embolism syndrome (FES)is a life-threatening complication in patients with trauma,especially in long bone fractures.The diagnosis of fat embolism is mainly clinical .The significance of the FES is that it has no specific laboratory findings nor specific treatment except supportive care,although it can be prevented by early fixation of the fractured bone.

Here we report a case which occurred immediately after the surgical fixation is done .We report a case of twenty days old fracture neck of femur which was diagonised as FES on the basis of clinical findings as per GURD and WILSON criteria.The patient received supportive management and a short course of intravenous methylprednisolone.

INTRODUCTION:

FAT EMBOLISM SYNDROME :

The incidence of fat embolism can approach upto 90% in patients with sustained injuries.If it affects,it can affect multiple organ system with its systemic inflammatory cascade resulting in high morbidities and mortalities.So early diagnosis and management is important.The diagnosis of FES is mainly clinical,depends upon clinical signs like dyspnoea,petechia,cognitive dysfunction in the first few days of trauma specially long bone fracture or intramedullary surgery.FES occurs 2-5%of patients who have long bone fracture.Studies says if diagonised early and treated promptly,the mortality may go down to 10%.GURD and WILSON CRITERIA mentioned below is one of the important tool to diagonise FES.

GURD and WILSON CRITERIA(published in 1974):

Major criteria:

1. Symptoms and radiological evidence of respiratory insuffiency(hypoxemia PaO2<60,FiO2=0.4)
2. Cerebral sequelae unrelated to head injury or CNS depression disproportionate to the level of hypoxia.
3. Petechial rashes

Minor criteria:

1. Tachycardia(>110/min)
2. Pyrexia(>38.5 degree C)
3. Retinal emboli on fundoscopy
4. Renal dysfunction(oligoanuria)
5. Jaundice
6. Acute drop in haemoglobin >20%
7. Sudden thrombocytopenia >50%
8. Elevated ESR(>70 mm 1 st hr)
9. Fat macroglobulinemia,fat globules in sputum.

Therefore,It was thought to be reported because it’s a very rare entity and also because of its diificulty in diagonosis as well as if at all diagonised early can lead to prevention of lot of complications and reduction in mortality.

CASE REPORT:

A patient 72 year male,a chronic ethanolic was admitted with the alleged history of fall followed by right trochanteric fracture .Initially after the fall,he was at home but later after 20 days ,he went to a local hospital where he was operated for the fracture.On the day of operation,he developed altered sensorium immediately after the surgery.He was shifted to an another local hospital with ICU facilities where he was transfused with 16 units of FFP and 2 Units of PRBCs for his deranged PT/INR and Low Hemoglobin level.Later when the condition of the patient further deteriorated,he was shifted to our tertiary care hospital for further management of the case.

On admission to our hospital,the patient was in altered sensorium,drowsiness(E2V2M5) and respiratory distress.Initially it was presumed to be a case of hepatic encephalopathy with ARDS,TRALI with AKI and deranged LFT. He was immediately put on invasive ventilation and shifted to Intensive Care Unit.

CXR ,ABG were done suggestive of ARDS.Bronchoscopy was done and lavage was taken and sent for analysis.Trop I was normal(0.098) with normal ECG and normal ECHO.Gradually the patient went into shock and inotropes were started.His platelet count came down to 75000,LDH was 570 and direct coombs test was positive.There was oozing from multiple iv puncture sites and petechial rashes spread all over his body.his urine output gradually decreased.Brochoscopy lavage showed pseudomonas and wound culture from his Bedsore showed acinetobacter growth(MDR).Antibiotics were revised as per hospital antibiogram .

Since there is neurological impairement,respiratory insufficiency with rashes all over the body along with acute drop in platelets count with haemoglobin and there was fat globules in urine ,it was thought to be a case of FAT EMBOLISM SYNDROME(FES) as per GURD and WILSON CRITERIA.

Injectable methylprednisolone was started with iv albumin.there was growth of yeast cells in the urine,so inj Anidulafungin was also started.Gradually the TC count of the patient came down,FiO2 decreased to 40%,inotropes support reduced and the patient was extubated on eighth day.His D- dimer and FDP came positive.Later the patient significantly improved and was shifted to the ward.

INVESTIGATIONS:

Hb:5.9,TLC:32.9,Plat:75000,PT(T):19.5,PT©:13.2,INR:1.56,Na:149,K:3.09,Creat:1.4,BUN:65,Bil:1.37, LDH:570, Albumin:2.5,Fibrinogen:Low,D-dimer positive,stool for occult blood positive,

UGIE:pangastritis,USG whole abdomen:liver parenchymal changes with bright kidneys,ascites.Urine for fat globulin positive,CT brain:normal except age related atrophy.Coomb,s test positive(direct).ECG:normal sinus rhythm,ECHO:normal,TropI:Normal(0.098),CXR:B/L diffuse infiltrates.

Bronchoscopy lavage(BAL)positive for pseudomonas,Bedsore swab culture positive for acinetobacter.Urine positive for budding yeast cells(heavy).

DISCUSSION:

FES is a rare but potentially life threatening complication.A high level of suspicion should be taken when patients present with hypoxia,confusion or rash within 24-72 hrs following long bone fractures and/or  postoperatively. Features of multisystem dysfunction occurs due to either(1)mechanical obstruction of capillaries by fat emboli or (2)production of toxic free fatty acids by hydrolysis of fat after trauma.

Close differential diagnosis include pulmonary embolism,acute respiratory distress syndrome,pulmonary edema or atypical infections.

The mainstay of treatment is always supportive;ensuring good arterial oxygenation,maintaining adequate intravascular volume. Prevention of FES includes early stabilisation of long bone fractures and prophylactic corticosteroids. Possible beneficial effects of steroids include stabilisation of the pulmonary capillary membrane,thus reducing interstitial edema,blunting the inflammatory response, stabilising complement activating system,and reducing platelet aggregation.Heparin is known to clear lipemic serum by stimulating lipase activity.

Without specific tests and validated criteria,diagnosis of FES is challenging.Although many patients recover fully if treated timely.Early diagnosis and and treatment is of paramount importance for a successful outcome.

REFERENCES:

1. Medscape-fat embolism
2. Fulde GW,Harrison P.Fat embolism-a review.ARCH EMERG MED.1991 Dec.8(4):233-9.
3. Mellor A,Soni N.Fat embolism.anaesthesia.2001 Feb,56(2):145-54.

Author:

Dr.Bhaskar jyoti Hazarika.
MBBS. DNB. CCEBDM, Junior Consultant,Critical Care Medicine
Narayana superspeciality hospital, Amingaon, Guwahati, Assam

The post A Rare Case of Fat Embolism Syndrome appeared first on CCEM Journal.

Invassive fungal infection is a common problem faced in ICU’s of all over the world.If we went back to history, It started in 1835 by the discovery of a mould , beauvariabassiana by Agostino Bassi. Then Gruby discovered candidiasis (1842) and Sluyter discovered aspergillosis in 18471,2. The candida albicans was the most predominant yeast in ICUs, which is recently changing to non albicans. 3

Aims and Objectives:

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

Materials and Methods:

All the positive cultures of respiratory, urine and blood samples were taken. The duration is from June’2017 till March’2018. A total of 86 positive samples were taken. We will continue to collect data’s and will come up with larger no in future.

Results:

Discussion and Conclusion:

The commonest fungus found in our study is Candida Albicans (65.12%), followed by Candida Tropicalis (15.12%), Candida Glabrata (6.98%) and Aspergillus Fumigatus (6.98%). There is 2 case of Candida Krusei (2.33%) and both are resistant to fluconazole. 1 case of C. Glabrata is intermediately sensitive to caspofungin. There are 1 case each of Candida parapsilosis , Candida Kefyr and Trichosporon Asahi were found. Candida tropicalis is found to be in second position. The third common position is shared by Candida Glabrata and Aspergillus Fumigatus. So Aspergillus Fumigatus is still an important pathogen in this part of India. Emerging fluconazole resistant in albicans and Krusei is an important finding as caspofungin decreased sensitivity to Glabrata.

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

References:

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

Author:

Dr.Apurba Kumar Borah, HOD, Critical Care and Emergency Medicine
Dr. Vicky Lahkar, Consultant Microbiologist
Narayana Superspeciality Hospital, Amingaon, Guwahati, Assam

The post Epidemiology of Fungal infection in a tertiary care hospital in Northeast India: A Retrospective Study [PART II] appeared first on CCEM Journal.

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

Case Report :

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

Discussion:

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

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

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

Conclusion:

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

Reference :

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

Author:

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

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

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

Case report:

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

Discussion:

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

Conclusion:

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

References:

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

Author:

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

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

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

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

Case report:

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

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

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

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

ABG DIFFERENCES PRE-PONE AND POST-PONE

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

Discussion:

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

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

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

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

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

Conflicts of interest:

All authors have none to declare.

References:

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

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

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

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

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

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

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

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

Author:

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

The post Prone Ventilation In Severe Ards appeared first on CCEM Journal.

Leptospirosis is a widespread and prevalent zoonotic disease. It occurs in both temperate and tropical regions; the incidence in the tropics is approximately 10 times higher than in temperate regions.In the tropics, leptospirosis is mainly a disease of poverty (including low education, poor housing, absence of sanitation, and poor income) [5]. It is acquired through occupational exposure (subsistence farming) and living in rodent-infested, flood-prone urban slums [6]. We report an unusual presentation of leptospirosis in a patient who presented to the Emergency Department (ED) with yellowish discoloration of the body and decreased urine output.

Introduction:

Leptospirosis is a widespread and prevalent zoonotic disease. It occurs in both temperate and tropical regions; the incidence in the tropics is approximately 10 times higher than in temperate regions [1]. Leptospirosis is an underreported disease, and there are no reliable global incidence figures. A modeling exercise by the World Health Organization’s (WHO’s) Leptospirosis Burden Epidemiology Group estimated that there were 873,000 cases worldwide annually with 48,600 deaths [2]. The organism infects a variety of both wild and domestic mammals, especially rodents, cattle, swine, dogs, horses, sheep, and goats. Rodents are the most important reservoirs for maintaining transmission in most settings.[3]. Human infection usually results from exposure to environmental sources, such as animal urine, contaminated water or soil, or infected animal tissue. Portals of entry include cuts or abraded skin, mucous membranes, or conjunctivae. The infection may rarely be acquired by ingestion of food contaminated with urine or via aerosols. Controversy exists as to whether Leptospira can penetrate the intact skin. [4]. We report an unusual presentation of leptospirosis in a patient who presented to the Emergency Department (ED) with yellowish discoration of the body and decreased urine output.

Case report:

A 35 years old male patient, farmer by occupation, presented in the ED with complaint of fever, nausea and vomiting for 6 days which was associated with history of yellowish discoloration of the body and decreased urine output. History of alcohol intake for the past 15 years was also present. The blood pressure was 130/80 mm of hg and PR was 110 bpm. General physical examination was remarkable for icterus and conjunctival suffusion. Systemic examination was apparently within normal limits(WNL). ABG was suggestive of metabolic acidosis ( Ph: 7.15, HCO3: 7, Pco2: 21, Na: 120, K: 2.8). ECG in the ED was WNL. Provisional diagnosis of leptospirosis, malaria and dengue was kept with due consideration to other atypical infections like scrub typhus and chikungunea fever. Patient was given empirical antibiotics (including coverage for leptospira) and antimalarials. Initial lab reports were suggestive of severe sepsis and hepatorenal dysfunction. (Refer to table 1). As per the lab reports the antibiotic support was escalated. Dengue (NS-1 antigen and Ig M) and malaria tests (Antigen and peripheral blood smear) were negative on day 2 of admission. Antimalarials were stopped. Howeveer despite antibiotic escalation there was progressive worsening of sepsis, renal and heatic dysfunction, although patient was hemodynamically stable. Serum procalcitonin was more than 75 IU/ml. In view of deranged renal function patient was given 2 sessions of hemodialysis. Final Blood and urine cultures reports did not show any growth of bacteria. In the mean time USG and later on CT abdomen (non contrast) reports were s/o acute pancreatitis. Conservative approach was followed.An upper GI endoscopy was done which revealed oesophageal candidiasis. Considering the critical state of the patient and non recovery of sepsis, a possibility of systemic fungal infection was kept and parentral antifungal agent (Mikafungin) was started. On day 5 leptospira Ig M report came to be positive. Chikungunea and scrub typhus (Weil Felix test) tests were negative. Gradually sepsis, renal and liver functions started resolving and patient was discharged with normal renal function and near normal liver function.

Table 1

Discussion:

In the tropics, leptospirosis is mainly a disease of poverty (including low education, poor housing, absence of sanitation, and poor income) [5]. It is acquired through occupational exposure (subsistence farming) and living in rodent-infested, flood-prone urban slums [6]. These are often associated with increased rainfall or flooding, which presumably increased the risk of exposure to contaminated water [7-11]. This case of leptospirosis was unusual because though the diagnosis of leptospirosis was straight forward clinically, the recovery was delayed because of underlying fungal infection. Leptospirosis presenting along with fungal infection is an unusual presentation.

REFERENCES:

1. Hartskeerl RA, Collares-Pereira M, Ellis WA. Emergence, control and re-emerging leptospirosis: dynamics of infection in the changing world. ClinMicrobiol Infect 2011; 17:494.
2. World Health Organization. Global burden of human leptospirosis and cross-sectoral interventions for its prevention and control. http://www.pmaconference.mahidol.ac.th/dmdocuments/2013-PMAC-Poster-P9-Bernadette%20Abela-Ridder.pdf (Accessed on August 13, 2013).
3. Ko AI, Goarant C, Picardeau M. Leptospira: the dawn of the molecular genetics era for an emerging zoonotic pathogen. Nat Rev Microbiol 2009; 7:736.
4. Stern EJ, Galloway R, Shadomy SV, et al. Outbreak of leptospirosis among Adventure Race participants in Florida, 2005. Clin Infect Dis 2010; 50:843.
5. Jesus MS, Silva LA, Lima KM, Fernandes OC. Cases distribution of leptospirosis in City of Manaus, State of Amazonas, Brazil, 2000-2010. Rev Soc Bras Med Trop 2012; 45:713.
6. Reis RB, Ribeiro GS, Felzemburgh RD, et al. Impact of environment and social gradient on Leptospira infection in urban slums. PLoSNegl Trop Dis 2008; 2:e228.
7. Kawaguchi L, Sengkeopraseuth B, Tsuyuoka R, et al. Seroprevalence of leptospirosis and risk factor analysis in flood-prone rural areas in Lao PDR. Am J Trop Med Hyg 2008; 78:957.

Author:

1. Dr. Shashank Gupta, Consultant Nephrologist (Narayana Superspeciality Hospital, Guwahati)
2. Dr. Apurba Kumar Borah, Consultant and HoD, Critical Care Medicine (Narayana Superspeciality Hospital, Guwahati)

The post An Unusual Case Of Leptospirosis: A Case Report 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.

Setting: Lung cancer clinic, Tertiary care hospital, Delhi, India

Objectives:

 To determine,

• The characteristics of patients diagnosed with lung cancer,
• Measure the time taken and the delays in the diagnosis and treatment of lung cancer and
• Assess possible causes for these delays.

Design:

A retro-prospective cross-sectional study based on detailed interview and review of treatment records of patients consecutively diagnosed with lung cancer which has been confirmed on cytology and/or histology.

Results:  

82.7% (out of 1020 patients) were male, 57% wereilliterate, and 78% were of lower socio-economic status, with 78.3% having history of smoking, while among non-smoker 55% had history of passive smoking. Chronic obstructive pulmonary disease was the commonest co-morbid disease.869 (85.2%) had Non- Small cell carcinoma, out it 41.8% were Squamous cell carcinoma and 35.7 % were Adenocarcinoma.

The total median delay from symptoms to treatment was 124 days, with the highest delay being at the level of general practitioner (median 80 days). 65.3% (of total 1020 patients) were misdiagnosed as PTB on initial visit to physician and were started on ATT empirically based on CXR.  77.2% of these were in stage IIIB and above (non-surgical stage), while 17.5% in stage IIIA on presentation to us.

Conclusion: 

There are unacceptable delays from symptom onset to initiation of treatment in lung cancer patients in India. Misdiagnosis of PTB is an important contributing factor. These delays need to be shortened to improve the detection of lung cancer at earlier stages.  High degree of suspicion should be kept in chronic smoker for presenting chest complains. Passive Smoker should not be labelled as non-smoker and high degree of suspicion kept for lung cancer among them.

Author:

• Dr Abhishek Agarwal, (Former Post- Graduate Student ,National Institute of Tuberculosis and Respiratory Diseases, Delhi.)
• DrAnand Jaiswal, (Former Consultant, Grade 1 , National Institute of Tuberculosis and Respiratory Diseases, Delhi.)
• Dr Vikram Vohra, (Chief Medical Officer, SAG, National Institute of Tuberculosis and Respiratory Diseases, Delhi.)
• Dr J K Saini, (Consultant, Grade 1, National Institute of Tuberculosis and Respiratory Diseases, Delhi.)

The post Delay in diagnosis and treatment in lung cancer patients appeared first on CCEM Journal.

The Case:

A 21 years old young man was presented to ER at 4 AM with an alleged history of RTA (Road Traffic Accident) , following which he had been in altered sensorium. On evaluation by ER physician and neurosurgeon, he was found to have a large left sided acute SDH (Subdural Hematoma) with midline shift and brainstem distortion. His BP was 130/90 mmhg, Pulse 88/min and Hb 10 gm%. He had also fracture left radius. Other systemic examinations were found to be satisfactory. He underwent emergency craniotomy at 8 AM. At the leg end of the surgery he suffered a cardiac arrest. Patient was revived, ROSC achieved after CPRand shifted to ICU after surgical closure of the craniotomy site. ABG revealed respiratory alkalosis with low haematocrit ( Hb was 3 gm%). Immediate bedside USG revealed hemoperitonium with multiple splenic lacerations. Urgent laparotomy was done and splenectomy performed. Massive blood transfusion was given according to protocol. After shifting back to ICU patient became hemodynamically stableand vasopressins were gradually tapered off. On Post-operative day 1 his sensorium improved satisfactorily. He was shifted from ICU on post-operative day2.  Post-operative day 3 he underwent ORIF (open reduction and internal fixation) with plating for fracture left radius. He recovered well and discharged on post-operative day 10. Later on he underwent elective cranioplasty.

Discussion:

Left upper quadrant pain, Kehr’s sign ( shoulder pain due diaphragmatic irritation by hemoperitonium ) , guarding and rebound tenderness are usually classical presentation of splenic trauma^2,3. But in some situations especially in case of polytrauma or when patient is in altered sensorium these classical findings may be totally absent as in our case. So in trauma cases there should be a high degree of suspicion of injury to other organ system as well. Meticulous hemodynamic monitoring remains the cornerstone in these cases. A low threshold for imaging modalities and multidisciplinary team approach is very much essential in dealing with such disasters.

References:

1. McIndoe, Archibald H. “Delayed haemorrhage following traumatic rupture of the spleen.” British Journal of Surgery78 (1932): 249-268.
2. Farhat GA, Abdu RA, Vanek VW: Delayed splenic rupture: real or imaginary?.Am Surg. 1992, 58: 340-345.
3. Kodikara S: Death due to hemorrhagic shock after delayed rupture of spleen: a rare phenomenon. Am J Forensic Med Pathol. 2009, 30: 382-383. 10.1097/PAF.0b013e3181c03caf.

Author:

1. Dr.Saikat Mallik (Consultant, Laparoscopic & Transplant Surgery Narayana Superspeciality Hospital, Guwahati)
2. Dr. Apurba Kumar Borah (Consultant & HOD, CCEM, Narayana Superspeciality Hospital, Guwahati)

The post Polytrauma: Can be anything appeared first on CCEM Journal.

Introduction:

Pressure ulcers have been described as one of the most costly and physically debilitating complications since the 20^th century. Pressure ulcers are a serious health issue for patients in all kinds of health care settings and even at home thus reduction of pressure ulcer prevalence in long-term care. Pressure ulcers are the common conditions among patients hospitalized in acute and chronic care facilities and impose significant burden on patients, their relatives and caregivers.

Hemodynamic instability, immobility, and limited nutrition increase the risk for pressure ulcer development among critically ill patients. The prevention of pressure ulcers can be a clinical challenge. The pain and discomfort due to pressure ulcer prolongs illness, rehabilitation, time of discharge and even contribute to disability and death.

Purpose:

The purpose of the quality improvement project was to reduce the occurrence of pressure ulcer in Narayana Superspeciality Hospital, Guwahati as there was increased incidence of pressure ulcer in prolonged stayed patient. The aim was to assess knowledge, practice and factors associated with pressure ulcer prevention among nurses in Narayana Superspeciality Hospital, Guwahati.

Objective of the Project:

To systematically review the incidents & find the interventions to prevent pressure ulcers.

Benchmark for Comparison:

Benchmark as a rate of three (3) was adopted from Indian society of critical care medicine.

Methodology:

Study Setting: NH Narayana Superspeciality Hospital, Guwahati.

Period: 5 months (July to November 2016) & all in-patients were included during that period.

Data Collection Tool: Daily Surveillance form of pressure ulcer.

Data Analysis:

Problem Associated with Development of Pressure Ulcer:

• Nurses were not following position changing protocol.
• Air mattresses for vulnerable patients for pressure ulcers were not applied, applied only after developing ulcers.
• Un-availability of adequate numbers of air mattresses.
• Meticulous care of patients where frequent skin care is advisable but not followed.

Intervention:

• Periodic training conducted for nurses in the hospital including expert from outside.
• Numbers (30%) of air mattress was increased for use.
• All in-patients are assessed for skin integrity in each shift by using Braden scale.
• Nurses are empowered (administrator approval) to decide for application of air mattresses.

Pressure Ulcer Status after intervention:

Recommendations for continuity of Quality of Care:

• Refresher & continuous training to all nurses on management of pressure ulcer.
• Appropriate assessment of vulnerable patients for pressure ulcers.
• Optimize nutritional status.
• Instant reporting of pressure ulcer at the first degree.

Author:

1. Ms Pinaki Bayan, (Nursing Superintendent, Narayana Superspeciality Hospital, Guwahati)
2. Ms Oinam Bidyalaxmi, (Quality Nurse, Narayana Superspeciality Hospital, Guwahati)
3. Ms Dimpimoni Kakoti, (Nursing Educator, Narayana Superspeciality Hospital, Guwahati)

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