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MBBS, MD (Pathology),
Sanjay Gandhi institute of trauma and orthopedics,
Bengaluru.
On Aug 2018




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Dr. Mamta Gupta
Consultant
(Ex HOD Obs &Gynae, Hindu Rao Hospital and associated NDMC Medical College, Delhi)
Aug 2018




Dr. Rajendra Kumar Ghritlaharey

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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)
E-mail: drrajendrak1@rediffmail.com
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.
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Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011
Anuradha

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
E-mail: anuradha2nittur@gmail.com
On Jan 2020

Important Notice

Case report
Year : 2023 | Month : June | Volume : 17 | Issue : 6 | Page : YD01 - YD03 Full Version

Seizure-Induced Coma in Patient with Haemoglobin 1.3 gram per decilitre and Multi-Organ Dysfunction: A Rare Case Report


Published: June 1, 2023 | DOI: https://doi.org/10.7860/JCDR/2023/63027.17978
Shrdhha Agrawal, Akhilesh Singh Parihar, Charuta Gadkari

1. Undergraduate, Department of Emergency Medicine, Jawaharlal Nehru Medical College, Wardha, Maharashtra, India. 2. Senior Resident, Department of Emergency Medicine, Acharya Vinobha Bhave Rural Hospital, Wardha, Maharashtra, India. 3. Professor, Department of Emergency Medicine, Acharya Vinobha Bhave Rural Hospital, Wardha, Maharashtra, India.

Correspondence Address :
Shrdhha Agrawal,
DMIMS, Indira Hostel, Sawangi, Wardha, Maharashtra, India.
E-mail: shrdhhaagrawal@gmail.com

Abstract

People of all ages are affected by anaemia which is a serious global health problem. Iron Deficiency Anaemia (IDA) seems to be the most commonly occurring type of anaemia in women. Elderly people with anaemia have higher morbidity and mortality. The purpose of treatment is to tackle the disorder’s underlying cause. Older people with persistent anaemia may need regular blood transfusions. The authors present a case report of a 55-year-old woman who visited the Emergency Department with primary complaints of convulsions and subsequent unconsciousness. She had generalised oedema and weakness since eight days. On examination, she was afebrile with pulse rate of 92 beats/min, Systolic Blood Pressure (SBP) of 80 mmHg. Laboratory results showed haemoglobin of 1.3 g/dL, increased White Blood Cells (WBC) and peripheral smear showed pencil-shaped cells and teardrop cells. Radiological investigation showed grade III renal parenchymal disease, cirrhosis of liver, gross ascites with bilateral pleural effusion, and splenic cyst. A 2D Echocardiography was done, which was suggestive of left ventricular hypertrophy, mild to moderate systolic dysfunction, along with dilated left ventricle. She was intubated in view of low Glasgow Coma Scale (GCS) and unconsciousness. On further stay in the hospital, she received blood transfusion. Hence, this case is a rare finding of severe anaemia.

Keywords

Anaemia, Iron deficiency, Multiple organ dysfunction syndrome, Sepsis

Case Report

A 55-year-old female patient, suffering from bronchial asthma since six years, was brought to the Emergency Department by the relatives with chief complaint of seizures, followed by unconsciousness. She had two episodes of convulsions on the same morning, which were associated with frothing, up-rolling of eyeball, and tonic clonic movement of both upper and lower limbs. There was a history of oedema all over the body, and generalised weakness since eight days. There was no history of chest pain, palpitations, cough, cold, fever, loose stools, or syncope. There was no information on whether the patient had hypertension, diabetes, or tuberculosis.

She was a known case of bronchial asthma and renal disease for which she was not taking any medication due to low socio-economic condition. There was a history of blood transfusion two years back, but no documentation was available.

On admission, the patient’s Glasgow Coma Scale (GCS) was 5 (E1V1M3). She was afebrile, with pulse rate of 92/min, Systolic Blood Pressure (SBP) of 80 mmHg. There was pallor and generalised oedema all over the body. On auscultation, S1 and S2 heart sounds were normal, breath sounds were diminished but equal on both sides, bilateral crepitations were present. Abdomen was soft and non tender on palpation. Patient was drowsy, responding to deep pain stimulus (grimacing present), corneal reflex was absent, bilateral pupils were mid dilated and reactive to light, deep tendon reflexes were slow and sluggish.

In view of low GCS 5, falling saturation, tachycardia, tachypnoea and gasping state, patient was intubated and taken on mechanical ventilator. A preliminary diagnosis of cardiogenic versus nephrogenic pulmonary oedema was considered at this point. Complete Blood Count (CBC), Liver Function Test (LFT), Kidney Function Test (KFT) and Arterial Blood Gas (ABG) analysis were done.

Drugs used were Inj. Midazolam 3 mg, Inj. Vecuronium bromide 6 mg Intravenous (i.v.). The patient’s blood investigations are shown in (Table/Fig 1).

(Table/Fig 2) represents the peripheral smear which shows pencil-shaped cells (Elliptocytes) and teardrop shaped cell (Dacrocyte-A type of poikilocyte).

(Table/Fig 3) shows the results of the KFT and (Table/Fig 4) shows the results of the blood coagulation profile and LFT. The purpose of ABG analysis was to arrive at the cause of unconsciousness, which could be respiratory in the form of severe hypoxia or CO2 narcosis or a metabolic cause.

Approximately two millilitre of yellowish ascitic fluid was withdrawn in a clot activator vacutainer. On wet mount, Red Blood Cells (RBCs) were 6.7 RBCs/High Power Field (HPF), WBCs-plenty of cells/HPF Total Leucocyte Count (TLC) was approximately 2992 cells/cu mm. Differential Leucocyte Count (DLC) have polymorphs 75%, lymphocytes 25%. The purpose of this investigation was to rule out sepsis.

Ultrasonography (USG) of the abdomen and pelvis was done, which was suggestive of grade III renal parenchymal disease according to USG grading of echogenicity of renal cortical disease, cirrhosis of liver, gross ascites with bilateral pleural effusion, and splenic cyst.

A 2D Echocardiography was done, which was suggestive of left ventricular hypertrophy, mild to moderate systolic dysfunction, along with dilated left ventricle.

Treatment at the Department of Emergency Medicine:

Initially, the patient was started on:

1) Inj. levetiracetam 1 g in 100 mL Normal Saline (NS)
2) Inj. noradrenaline 10 mL/hr.
3) Inj. hydrocortisone 100 mg i.v.
4) Inj. sodium bicarbonate 100 mL
5) Inj. calcium gluconate 10 mL was given for correction of acidosis and hyperkalaemia. Further, she was admitted to the Intensive Care Unit (ICU).

Under all aseptic precautions, and USG guidance, a 3-lumen Central Venous Catheter (CVC) was inserted through the left internal jugular vein for guiding fluid management and administration of drugs.

Treatment in ICU: The patient was started with antibiotics such as inj. piperacillin and tazobactam 2.25 g i.v. TDS, inj. levofloxacin 500 mg i.v. OD. Acidosis and hyperkalaemia were corrected with i.v. glucose insulin infusion and inj. sodium bicarbonate 210 mEq, inj. calcium gluconate 20 mL were given. In view of severe anaemia, the patient received four units of packed Red Blood Cells (pRBC). In view of deranged coagulation profile, the patient was transfused with five units of Fresh Frozen Plasma (FFP). From the point of view of severe hypotension, inotropic supports were continued.

She continued to be on mechanical ventilation and could not be considered for weaning as the condition kept on deteriorating in spite of the treatment and she died in the ICU on the 4th day with cardiogenic shock due to severe anaemia with cirrhosis of liver and Chronic Kidney Disease (CKD). The diagnosis of the patient was Multiple Organ Dysfunction Syndrome (MODS) secondary to cardiogenic shock with CKD along with underlying chronic severe anaemia.

Discussion

Anaemia affects one third of the total community, contributing to increased morbidity and mortality, decreased work productivity, and impaired neurodevelopment (1). Recently, research has increased the understanding of the complex aetiology of anaemia, including prevalence of anaemia due to Iron Deficiency (ID) and its effect on inflammation and infection. An approach for determining the aetiology, including the patient’s past medical record as well as laboratory testing of the number of reticulocyte, serum ferritin and CRP, serum vitamin B12, RBC, folic acid, and serum creatinine. Microcytosis is an indication of inadequate haemoglobin synthesis, which can be brought about by either iron deficit or the congenital condition, haemoglobinopathy. Macrocytosis is the consequence of an interruption of division and maturation of pro-erythroblasts in the bone marrow, e.g., due to vitamin B12/folic acid deficiency or drinking too much alcohol (2).

This patient presented with severe life-threatening anaemia with Hb of 1.3 g/dL. To the best of the authors’ knowledge, this is the minimum haemoglobin level reported in the literature. Chronic anaemia can be life-threatening and can even cause death. Untreated anaemia can lead to multiorgan failure. In early phases, body can compensate through non haemodynamic and haemodynamic mechanisms (3). A case of severe anaemia with Hb of 1.8 g/dL had been reported in 2016 where the patient had generalised fatigue, and palpitations at presentation. He was diagnosed to have carcinoma of the colon with presence of occult blood in the stool (4). There was no known source of bleeding in the present case. Another case reported with a Hb value of 1.4 g/dL where the patient had fatigue and dizziness and suffered a fall. She had irregular menstrual bleeding for over three decades and did not seek medical help (5). Similarly in India, women tend to ignore seeking medical help. Nutritional factor is an important reason of anaemia in India.

Another case of severe anaemia with Hb of 1.7 g/dL has had been reported in 2005. However, the patient was a diagnosed case of bulimia nervosa with coeliac disease (6). A study based on haemoglobin level and blood transfusion in septic patients showed that anaemia is very common in septic patients. There are a number of mechanisms that indicate a rapid drop in haemoglobin levels in patients with sepsis. The major mechanism consists of a decrease in erythropoietin production due to release of inflammatory cytokines, such as Tumour Necrosis Factor-α (TNF-α), Interleukin-1 (IL-1), and Interleukin-6 (IL-6). Other possible mechanisms that contribute to the reduction in haemoglobin in sepsis are gastrointestinal bleeding/stress-induced haemophilia due to fluid overload, withdraw for laboratory analysis, altered iron metabolism, haemolysis as part of pathogenesis of some infectious processes, bleeding due to Disseminated Intravascular Coagulation (DIC) and possibly erythrocytosis destruction due to damage to the RBC membrane (7). A combination of anaemia and sepsis can impair tissue oxygenation.

Therefore, the treatment of patients with sepsis focuses on maximisation of oxygen delivery to tissues to treat cellular hypoxia and cell progression dysfunction for the purpose of preventing or delaying the onset of MODS (7). Elderly patients with anaemia often have significant co-morbidities, including heart failure and CKD (8). A study has shown that 5-year mortality is 2.4 times higher in anaemic men and 1.6 times higher in women compared to non anaemic patients. It should be noted that the increase in anaemiarelated mortality was found to remain unchanged after adaptation for pre-existing co-morbid conditions (9). The treatment for anaemia includes oral iron therapy, intravenous iron therapy and in chronic cases, blood transfusion. In this case, the patient presented with severe anaemia of 1.3 g/dL. The patient continued to be on mechanical ventilation and could not be considered for weaning as her condition kept on deteriorating in spite of treatment.

Conclusion

Severe anaemia can lead to life-threatening complications. This patient came in peri-arrest condition where oxygenation and circulatory support were a priority. Haemoglobin (Hb) of 1.3 g/dL could be a result of multiple medical factors, mainly nutritional, associated renal pathology, sepsis as well as social factors like lack of awareness and education, which are common in Indian scenario.

References

1.
Chaparro CM, Suchdev PS. Anaemia epidemiology, pathophysiology, and etiology in low-and middle-income countries. Ann N Y Acad Sci. 2019;1450:15- 31. https://doi.org/10.1111/nyas.14092. [crossref][PubMed]
2.
van der Lelie J, van Oers MH, von dem Borne AE. [Diagnostics for classification of anaemia]. Ned Tijdschr Geneeskd. 2001;145(18):866-69.
3.
Metivier F, Marchais SJ, Guerin AP, Pannier B, London GM. Pathophysiology of anaemia: Focus on the heart and blood vessels. Nephrol Dial Transplant. 2000;15:14-18. https://doi.org/10.1093/oxfordjournals.ndt.a027970. [crossref][PubMed]
4.
Schmitt RE, Buckley CJ. Extreme anaemia (hemoglobin 1.8 g/dL) secondary to colon cancer. Proc (Bayl Univ Med Cent). 2016;29(4):393-94. [crossref][PubMed]
5.
Chai AL, Huang OY, Rakoc? evic´ R, Chung P. Critical iron deficiency anaemia with record low hemoglobin: A case report. J Med Case Rep. 2021;15:472. https:// doi.org/10.1186/s13256-021-03024-9. [crossref][PubMed]
6.
Jost PJ, Stengel SM, Huber W, Sarbia M, Peschel C, Duyster J. Very severe iron- deficiency anaemia in a patient with celiac disease and bulimia nervosa: A case report. Int J Hematol. 2005;82:310-11. https://doi.org/10.1532/IJH97.E0505. [crossref][PubMed]
7.
Muady GF, Bitterman H, Laor A, Vardi M, Urin V, Ghanem-Zoubi N. Hemoglobin levels and blood transfusion in patients with sepsis in Internal Medicine Departments. BMC Infect Dis. 2016;16:569. https://doi.org/10.1186/s12879-016-1882-7. [crossref][PubMed]
8.
Price EA, Mehra R, Holmes TH, Schrier SL. Anaemia in older persons: Etiology and evaluation. Blood Cells Mol Dis. 2011;46:159-65. https://doi.org/10.1016/j. bcmd.2010.11.004. [crossref][PubMed]
9.
Izaks GJ, Westendorp RGJ, Knook DL. The definition of anaemia in older persons. JAMA. 1999;281:1714-17. https://doi.org/10.1001/jama.281.18.1714.[crossref][PubMed]

DOI and Others

DOI: 10.7860/JCDR/2023/63027.17978

Date of Submission: Jan 21, 2023
Date of Peer Review: Feb 11, 2023
Date of Acceptance: Mar 03, 2023
Date of Publishing: Jun 01, 2023

AUTHOR DECLARATION:
• Financial or Other Competing Interests: None
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. No

PLAGIARISM CHECKING METHODS:
• Plagiarism X-checker: Jan 25, 2023
• Manual Googling: Feb 20, 2023
• iThenticate Software: Mar 02, 2023 (4%)

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