Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

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Aug 2018

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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
On May 11,2011

Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
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Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."

Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
On April 2011

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.

Dr. Anuradha
On Jan 2020

Important Notice

Case report
Year : 2008 | Month : October | Volume : 2 | Issue : 5 | Page : 1107 - 1109

Respiratory Failure Secondary To Obstructive Uropathy

Abbas MT *, KhanFY**,Baidaa A***,Errayes M****, Haleem Al H Al*****

*(MD) (MRCP),** (MD),*** (MD), ****,*****Hamad General Hospital,P O Box 3050 Medical Deptt.Doha-Qatar

Correspondence Address :
Dr. MTAbbas (MD) (MRCP)Senior Specialist Deptt. of Medicine,Hamad general Hospital PO Box 3050, Doha-Qatar Tel: 009745220486,Fax 009744392273 E Mail:


A 34 year-old male patient who presented for the first time with quadriparesis and type 2 respiratory failure, was found to have severe hypokalaemia (1.1 mmol/L) associated with renal failure, normal anion gap metabolic acidosis and respiratory acidosis .Imaging studies showed left hydronephrosis secondary to urinary bladder neck obstruction. Diagnosis of respiratory failure due to hypokalaemia, which resulted from obstructive uropathy, was established.
After relief from obstruction and administration of intravenous fluid and oral potassium supplement, his renal function and his serum potassium level was normalized, and his condition improved. On one of the following days, the patient was discharged.


hypokalaemic paralysis, respiratory failure, obstructive uropathy.

Hypokalemaic paralysis is a medical emergency due to the risks of cardiac arrhythmia, respiratory failure, and rhabdomyolysis. Besides supplementing patients with potassium to hasten recovery, the astute physician must search for the underlying cause, to avoid missing a treatable and curable disorder. We report a 34 year old patient who presented with quadriplegia and then passed into respiratory failure secondary to hypokalaemic paralysis, which proved to be secondary to obstructive uropathy.

Case Report

A 34- year old Sri Lankan patient, not known to have any chronic disease before, presented to the Accident and Emergency Department of our hospital because of the inability to move his lower and upper limbs for one day . The patient admitted that he had difficulty in passing urine since the past one month, and had to strain to pass urine. He also had on and off vomiting for one month, which increased 2 days before admission. He denied fever, palpitation, previous similar attack, drug intake, or a family history of similar conditions. Upon examination, the patient was conscious, oriented, dehydrated, with a blood pressure of 102/62, a pulse rate of 80/minute, temperature of 37.2ÂşC and a respiratory rate of 26/minute. His chest, heart and abdomen were normal, apart from a distended urinary bladder. He had power grades, one in both upper and lower limbs, his reflexes were normal, and his planters were down going. There was no sensory deficit and his cranial nerves and ocular muscles were intact.

His investigations showed white blood cells: 18700/µL, haemoglobin: 12.2g/dl and platelets:368000/µL. Biochemistry showed potassium: 1.1 mmol/L, calcium: 1.8mmol/l, chloride: 94mmo/l, glucose: 6.6 mmol/l, creatinine: 523 µmol/L, urea: 26.7 mmol/l, bicarbonate: 15 mmol/l, sodium: 120 mmol/l, magnesium: 1.14 mmol/L, phosphorus: 1.37 mmol/L. Serum osmolality was 263 Os/kg, urine osmolality was 315 Os/Kg , myoglobin was 3308ng/ml, SGOT was 74U/L, , lactic acid was 1.19 mmol/L (0.5-2.2) and lactate dehdrogenase (LDH) was 1534U/L. His initial blood gas showed ph 7.136 pCO2 42.9 mm/Hg, PO2 91.1mm/Hg, oxygen saturation was 92.6% and electro cardiogram showed flat T wave with U wave. Urine examination showed pH 7, WBC 10/HPF; Myoglobin in urine was positive. Urine and blood culture was negative. Spot urine showed: Potassium 25 mmol/L with transtubular potassium gradient of 18.97, magnesium 1 mmol/l and chloride 48 mmol/l. 24 hours urine: Volume was 5104 ml/24 hr , creatinine was 7.5 mmol/L, creatinine clearance was 30ml/min(serum creatinine reach 175mmol/L), sodium was 194 mmol/L( Normal 27-287), potassium was 128 mmol/L(25-125), phosphorus was 31.64 mmol/L, magnesium was 5.1 mmol/L (3-5) and chloride was 245mmol/L (110-250). Free T4 was 15.2 and TSH was 4.19(normal).

The patient was admitted to the medical intensive care unit (MICU) as a case of hypokalaemic paralysis with possible renal tubular acidosis and renal failure. Trial of Foleys catheter insertion failed because of obstruction and so a supra pubic catheter was inserted, and the patient passed 800 ml of urine immediately. The patient was started on an intravenous fluid with a high dose of potassium through the central line followed by sodium bicarbonate. After a few hours, the patient became drowsy, and his arterial blood gas showed acute type 2 respiratory failure with PH 6.84, PCO2 115.7mm/Hg, PO2 158 mm/Hg and so the patient was intubated and initiated on a ventilator. During intubation, the patient passed about 4-5 liters/ day of urine daily, secondary to relief of obstruction, and had electrolyte disturbance with hypomagnesaemia, and hypophosphataemia for which he had replacement therapy. Moreover, he had 2 attacks of seizure for which he was given midazolam. After 5 days, his potassium and electrolytes improved, and he was extubated and started to move all four limbs.

Further Investigations
Renal Sonography showed: right kidney 8.5 × 4.2cm with dilated pelvis of 13 mm and left kidney measured 10.7×5.0 cm and 30 mm pelvic dilatation with distended urinary bladder and trace of perinephric fluid. Spiral computed tomography scan examination of abdomen and pelvis with delayed scan for urinary tract with intravenous contrast showed dilated extra renal pelvis of the left kidney with normal renal parenchyma (Table/Fig 1). Thus, as urethral stricture suspected, flow cytometry, urodynamic micturating cystourethrogram and ascending urethrography were not conclusive, so cystoscopy was done which showed trabeculated bladder with thickening of mucosal fold from verumontanum, ending distal to sphincter, almost occluding the lumen. So resection was done, and Foleys catheter was inserted. The patient’s condition improved and he was discharged in good condition with a Creatinine of 136mmol/l and a potassium level of 3.9 mmol/L.


The probable causes of hypokalaemia are either reduced intake of potassium, or trans cellular shift of potassium or loss of potassium (non renal or renal)(1).The well known causes of hypokalaemic paralysis (HP) are thyrotoxicosis, familial and sporadic hyperaldosteronism, gastrointestinal loss and renal tubular acidosis (RTA)(2).Gastrointestinal loss is usually evident from history, in addition to the laboratory test which shows low urine potassium.

Our patient did not have signs or symptoms of hyperthyroidism, as well as he had normal thyroid function test. Also, he had no family history, nor was his case sporadic, because of the electrolyte disturbance and high trans tubular potassium gradient.

In view of the above mentioned data, the most likely cause of hypokalaemia in this patient was renal tubular acidosis; it was found that patients with distal renal tubular acidosis had hypokalaemia in 28-53% of cases(4),(5). Potassium wasting is due to primary tubular defect(6). The presentation of the patient with hypokalaemic paralysis secondary to RTA cannot be differentiated from attacks of familial periodic paralysis. In both conditions, the muscle involvement can vary in severity from moderate muscle weakness to almost complete paralysis(3).A negative family history and high urine potassium make familial hypokalaemic paralysis unlikely.

Respiratory failure secondary to hypokalaemia is quite uncommon; a MEDLINE search showed that only few cases(7),(8),(9),(10),(11) of respiratory failure secondary to hypokalaemia have been reported in the literature.

This patient presented to the emergency department with combined metabolic and respiratory acidosis, but respiratory failure became very evident when he was given oxygen.

Emergency treatment of hypokalaemic paralysis due to renal tubular acidosis consists of intravenous potassium and bicarbonate therapy(2).Potassium should be replaced prior to bicarbonate therapy, because bicarbonate can precipitate further hypokalaemia due to intracellular potassium influx. Our patient was given potassium at the beginning and later on, he received bicarbonate. The definitive treatment is to treat the underlying cause; in our case , resection of the mucosal fold improved the condition.

In conclusion, this case highlights the significance of considering hypokalaemia as a significant cause of respiratory failure which needs prompt diagnosis and treatment to save the patient’s life.


. Singer GG, Brenner BM. Fluid and electrolyte disturbances. In: Harrison’s Principles of Internal Medicine. 16th ed. Kasper DL, Fauci AS, Longo DL, Braunwald B, Hauser SL, Jameson JL Eds. McGraw-Hill, New York, 2005: 258-63.
. Ahlawat SK, Sachdev A. Hypokalemic paralysis. Post Graduate Med J 1999; 75: 193-7.
. Koul PA, Saleem SM, Bhat D. Sporadic distal renal tubular acidosis and periodic hypokalaemic paralysis in Kashmir. J Intern Med1993; 233 (6): 463-6.
. Wrong OM, Feest TG. The natural history of distal renal tubular acidosis. Contrib Nephrol 21: 137, 1980.
. 3Caruana RJ, Buckalew VM. The syndrome of distal (type 1) renal tubular acidosis: clinical and labrotary in 58 cases Medicine 67:84,1988
. Sebastian A, McSherry E, Moris RC. Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in type 1 and 2 RTA despite sustained correction of systemic acidosis. J Clin Invest 50: 667, 1971.
. Gombar S, Mathew PJ, Gombar KK, D'Cruz S, Goyal G. Acute respiratory failure due to hypokalemic muscular paralysis from renal tubular acidosis. Anaesth Intensive Care. 2005 ;33:656-8
. Poux JM, Peyronnet P, Le Meur Y, Favereau JP, Charmes JP, Leroux-Robert C. Hypokalemic quadriplegia and respiratory arrest revealing primary Sjogren's syndrome. Clin Nephrol 1992 ;37:189-91
. Haddad S, Arabi Y, Shimemeri AA. Hypokalemic paralysis mimicking Guillain-Barre syndrome and causing acute respiratory failure. Middle East J Anesthesiol. 2004;17:891-7
. Le Corre A, Veber B, Dureuil B.An unusual cause of acute respiratory distress Ann Fr Anesth Reanim. 2000;19: 549-51
. Mishra I,MishraSK,PatiSS,Mohpatra DN: Renal Tubular Acidosis Presenting As Severe Hypokalemia With Respiratory Paralysis: Report Of Two Cases. The Internet Journal of Tropical Medicine. 2006: 3/1.

Tables and Figures
[Table / Fig - 1]
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