Research Connect

Sauparna, Dey

M D, Dr. Ravi

Digital Journal of Clinical Medicine 
Volume 2 Issue 2 Article 9 
1-1-2020 
A Case of Right Lower Lobe Lung Abscess with Stage III 
Empyema 
Dey Sauparna 
JSS AHER 
Dr. Ravi M D 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
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Recommended Citation 
Sauparna, Dey and M D, Dr. Ravi (2020) "A Case of Right Lower Lobe Lung Abscess with Stage III 
Empyema," Digital Journal of Clinical Medicine: Vol. 2: Iss. 2, Article 9. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of Right Lower Lobe Lung Abscess with Stage III Empyema 
 Dey Sauparna, Dr. Ravi M D 
 
CLINICAL HISTORY: 
 
A 5 yr old female child, hailing from Mandya, came with history of cough and fever since 2 
weeks. 
Child was apparently normal 2 weeks back following which she developed cough, insidious in 
onset, gradually progressive, sputum not blood stained. 
He also gives a history of fever, continuous, high grade. 
No history of respiratory distress. 
No other significant history. 
No known congenital anomalies. 
No history of previous surgeries. 
 
EXAMINATION AND INVESTIGATIONS: 
 
GENERAL PHYSICAL EXAMINATION: A female child, cooperative, moderately built and 
well nourished, appears well oriented to time, place and person. 
VITALS: 
BP: 100/70 mmHg 
PR: 140 beats/min 
RR: 50 breaths/min 
SpO2: 90%  at room air. 
No pallor, icterus, cyanosis, clubbing, oedema or generalized lymphadenopathy. 
RS- B/L AE+ 
Right side air entry reduced. Right course crepitus present. 
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Sauparna and M D: A Case of Right Lower Lobe Lung Abscess with Stage III Empyema
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PER ABDOMEN-Soft, non-tender. 
CVS: S1, S2 heard. No murmurs. 
CNS: No focal neurological deficit 
EXTERNAL GENITALIA: Normal 
BLOOD INVESTIGATIONS: 
HB: 11.3gms/dl 
TOTAL WBC:20880 cells/ml 
DLC: 
N:76.6%, L:18.4%, 
E:0.4%, M:4.4%, B:0.2% 
RBC: 4.14 million/ml 
PCV/HCT: 35.1% 
MCV:84.8fl 
MCH:27.3pg 
MCHC:32.2 gm/dl 
RDW-CV:14.8% 
PLATELET: 6.98lakh/ml 
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BIOPSY (SMALL SIZE <2cm) 
Right lung sloughed out tissue 
MACRO: Specimen consists of multiple grey white membranous tissue. Fragments altogether 
measure 5×3.5 cm (all embedded). 
MICRO: Sections show sheets of inflammatory cells consisting predominantly of neutrophils 
and few macrophages. Karyorrhectic debris, areas of haemorrhage and granulation tissue seen. 
No granulomas seen in the sections studied. Features are suggestive of acute suppurative 
inflammation. 
CHEST X RAY: 
AT THE TIME OF ADMISSION 
 
 
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Sauparna and M D: A Case of Right Lower Lobe Lung Abscess with Stage III Empyema
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AFTER TREATMENT 
 
 
CECT THORAX 
 
 
 
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CECT THORAX 
SURGERY: RIGHT DECORTICATION on 25.2.2020 under General Anaesthesia 
INTRA OP FINDINGS: Orange peel like pleural flakes 
FINAL DIAGNOSIS: Right Lower Lobe Lung Abscess with Stage III Empyema 
TREATMENT: 
Surgery : Right Decortication with insertion of ICD. 
Syrup LINEZOLID (100mg/5ml) 1-0-1x 7days. 
Syrup CEFPODOXIME(100mg/5ml) 1-0-1x7days. 
Syrup PARACETAMOL DS 4ml SOS for pain/fever. 
Incentive Sprirometry 
MUPIROCIN OINTMENT IP 5mg 2for L/A 1-0-1 for ICD wound. 
The patient was asked for follow up review in paediatric surgery OPD after 1 week. 
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Sauparna and M D: A Case of Right Lower Lobe Lung Abscess with Stage III Empyema
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DISCUSSION: 
Lung abscess represents necrosis and cavitation of the lung following microbial infection. 
Lung abscesses can be single or multiple but usually are marked by a single dominant 
cavity>2cm in diameter.(1) 
They are a significant source of mortality and morbidity even though their prevalence has 
decreased in the antibiotic era. They can be primary (80%) or secondary. Primary lung abscess 
occurs mainly by aspiration, caused by anaerobic bacteria, and in the absence of an underlying 
pulmonary or systemic condition. 
Secondary lung abscesses occur in the presence of an underlying condition such as an obstructive 
process (eg. Foreign body in bronchi or tumour) or a systemic process (eg. Immunocompromised 
conditions like HIV). Lung abscesses can also be characterised as acute (<4-6 weeks) or chronic 
(~40% of the cases). 
 
Clinical manifestations are initially similar to those of pneumonia, with cough, fever, sputum 
production, and chest pain; in chronic cases night sweats, fatigue and anaemia is often observed 
with anaerobic lung abscesses. 
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Some patients with putrid lung abscesses may have discoloured, foul smelling and foul-tasting 
sputum. Patients with lung abscesses due to aerobic organisms like S. Aureus, have a more 
fulminant course with high fevers and rapid progression. Physical examination shows fever, poor 
dentition, and/or gingival disease, amphoric or cavernous breath sound. Digital clubbing and the 
absence of gag reflex may be additional findings. 
Diagnosis is made by chest imaging. CT has a better definition and may provide earlier evidence 
of cavitation. 
The infection is most likely polymicrobial so non-invasive sputum collection and culture may 
not reveal anaerobic pathogen. Many physicians treat for anaerobic infection empirically by 
considering putrid smelling sputum as diagnostic. 
Parapneumonic pleural effusion (PPE) occurring in early-stage (stage I) pleural empyema (PE) 
can be managed by chest tube drainage, which should be performed as soon as possible, to 
achieve re-expansion of the pulmonary parenchyma. Chronic disease leads to fibrin deposits on 
both pleural surfaces (stage II), followed by a thickened pleura peel (stage III). (2) The 
compressed lung normally expands after drainage of fluid but if it fails to expand the surgical 
debridement and decortication is done either by Video assisted thoracoscopic surgery(VATS) or 
open technique(thoracotomy). 
In Decortication, the fibrous cortex or peel from entrapped underlying lung is removed so that 
the lung can expand to obliterate the pleural space. This is usually performed through a 
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Sauparna and M D: A Case of Right Lower Lobe Lung Abscess with Stage III Empyema
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posterolateral thoracotomy. It requires careful dissection to remove the parietal and visceral 
cortex, taking care not to damage the visceral pleura, so allowing the lung to re-expand fully.(3) 
REFERENCES: 
1. Jameson L, Fauci A, Kasper D, Hauser S, Longo D, Loscalzo J. Harrison’s Principles of 
Internal Medicine. 20th ed. Vol. 1. New York: McGraw-Hill Education; 2019. 919 p. 
2. [Decortication in Pleural Empyema: Reasonable Effects on Lung Function?]. – PubMed – 
NCBI [Internet]. [cited 2020 Mar 10]. Available from: 
https://www.ncbi.nlm.nih.gov/pubmed/27607885 
3. Williams N, O’Connell R, McCaskie W. Bailey & Love’s Short Practice of Surgery. 27th 
ed. Vol. 2. Boca Raton, FL: CRC Press; 2018. 923 p. 
 
 
 
 
 
 
 
 
 
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Sauparna and M D: A Case of Right Lower Lobe Lung Abscess with Stage III Empyema
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English

A Case of Right Lower Lobe Lung Abscess with Stage III Empyema

Munjal, Sahil

Digital Journal of Clinical Medicine 
Volume 2 Issue 3 Article 10 
1-1-2020 
A Case of Intertrochanteric Fracture 
Sahil Munjal 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Munjal, Sahil (2020) "A Case of Intertrochanteric Fracture," Digital Journal of Clinical Medicine: Vol. 2: Iss. 
3, Article 10. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of Intertrochanteric Fracture 
 Sahil Munjal, JSS Medical College, JSS AHER, Mysuru  
Clinical History 
A 70-year-old patient came with complaints of left hip pain for 4 days which occurred after 
sustaining a fall from height.  
The pain was sudden in onset progressive in nature. The pain was sharp, shooting in nature 
which increased on movement and decreased on rest. 
No history of any other symptoms 
Past History: Not a known case of Hypertension, Diabetes Mellitus, Asthma, Tuberculosis  
Examination and Investigations 
GENERAL PHYSICAL EXAMINATION: 
Pulse:86 beats per minute 
Blood Pressure: 130/80 mmHG 
Respiratory Rate: 18 breaths per minute 
Mild pallor present, no icterus, no clubbing, cyanosis, lymphadenopathy or edema noticed. 
SYSTEMIC EXAMINATION: 
PER ABDOMEN: 
Soft, non-tender, no free fluid present, normal bowel sounds heard. 
CVS:  S1, S2 heard, no murmurs. 
RS: NVBS heard, no added sounds. 
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Munjal: A Case of Intertrochanteric Fracture
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CNS: No focal neurological deficit 
LOCAL EXAMINATION: 
ATTITUDE: Patient present in supine position, no exaggerated lumbar lordosis, anterior 
superior iliac spine is at same level, the limb is in external rotation with knee, hip and ankle 
flexed. 
INSPECTION: 
Absence of swelling and redness, no wasting and no scars and sinuses. 
PALPATION: 
Local rise of temperature felt with presence of tenderness over the left greater trochanteric area. 
Active toe movements seen with no sensory deficits. 
Distal pulsations present. 
LABORATORY INVESTIGATIONS: 
Hb:6.9% 
WBC count:8,000 cu/mm 
X RAY: 
Following X-ray of the AP view of the pelvis shows the intertrochanteric fracture of the neck of 
the left femur with displacement  
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Hip X-Ray 
Final Diagnosis 
Intertrochanteric fracture of LEFT FEMUR 
 
Discussion 
CLASSIFICATION OF INTERTROCHANTERIC FRACTURE: Intertrochanteric 
(IT) fractures are commonly witnessed. 
 The classification of the IT fractures is important as it helps us choose from an array of implants 
for a better outcome and management protocols. 
Few classifications focus on the anatomical pattern (Evans; Ramadiers; Decoulx and Lavarde) 
while others on maintaining reduction of various types (Jensen’s modification of Evan’s Ender, 
Tronzo , AO). [1] 
Intertrochanteric fracture is the most common of the extracapsular hip fractures many of which 
may be associated with a varus deformity. Comminuted fractures may occur which may also 
manifest as separate fragments of either one trochanter or both of the lesser and greater 
trochanter.[2] 
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Munjal: A Case of Intertrochanteric Fracture
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FRACTURE HEALING:  
Fracture Healing occurs by callous formation and can occur by primary or secondary union. 
Healing by Primary Union: here the ends of the fractures are approximated by application of 
surgical clamps, metal plates. Herein the bony union occurs with the formation of medullary 
callous without the formation of periosteal callous. 
Healing by Secondary Union: It is more common and occurs upon application of plaster to the 
broken bone, the steps involved are: 
Procallous Formation: Hematoma that has occurred due to bleeding of blood vessels has blood 
and fibrin which forms granulation tissue. Local inflammatory response occurs which clears 
away the dead tissue and debris. Ingrowth of the granulation tissue occurs causing formation of 
callous composed of bony and cartilaginous material. 
Osseous Callous Formation: The procallous formed earlier acts as a scaffolding over which 
forms the osseous callous, the woven bone is taken over by formation of lamellar bone. 
Remodelling: 
Osteoblastic and osteoclastic activity occurs in the bone helping it remodel in such a way that 
after sometime the new bone formed looks indistinguishable from the normal bone. [3][4] 
Acknowledgements: None 
References 
GS Kulkarni, Rajiv Limaye, Milind Kulkarni, Sunil Kulkarni, Current Concept review: 
Intertrochanteric fractures Indian Journal Of Orthopaedics.2006;40:16-23. 
2. learning radiology .com 
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3. Textbook of Pathology by Harsh Mohan 8th edition. 
4. Textbook of Pathology by Robbins and Cotran 
 
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Munjal: A Case of Intertrochanteric Fracture
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A Case of Intertrochanteric Fracture

S.G, Dr Vaishnavi

P, Dr Shasthara

Digital Journal of Clinical Medicine 
Volume 2 Issue 5 Article 6 
1-1-2020 
“Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT 
SYNDROME 
Dr Vaishnavi S.G 
JSS AHER 
Dr Shasthara P 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
S.G, Dr Vaishnavi and P, Dr Shasthara (2020) "“Hunting” a case of External Ophthalmoplegia: TOLOSA-
HUNT SYNDROME," Digital Journal of Clinical Medicine: Vol. 2: Iss. 5, Article 6. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
“Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROME 
Dr Vaishnavi.S.G, 7th Term MBBS  
Dr Shasthara P , Assistant Professor, Department of Neurology, JSS Medical College,JSS 
AHER,Mysuru  
Clinical History 
A 35-year-old female, who is a housewife, hailing from Mysuru district came with 
complaints of pain in the left eye, sudden in onset, retro-orbital, dull aching, continuous, 
radiating to the left hemicranium since 15 days. One week later, she developed  diminution of 
vision in the left eye which was insidious in onset and progressive. 
The patient also complained of diplopia since 15 days. 
The patient complained of numbness on the left side of the forehead since a week. 
The patient had no h/o  photo-phobia, phonophobia, nausea, or vomiting. 
No h/o excessive watering of eyes, drooping of eyelids, painful eye movements. 
No h/o similar complaints in the past. 
Examination 
A middle-aged woman, moderately built, and nourished is conscious, co-operative, well 
oriented to time, place, and person. 
Vitals- 
PR: 84bpm, BP: 120/80mm Hg, RR: 20cpm, Temperature: Afebrile 
No pallor/icterus/cyanosis/clubbing/lymphadenopathy/edema 
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S.G and P: “Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROM
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Central Nervous System- 
Higher Mental functions: Conscious and oriented. 
Cranial Nerves: 
Optic nerve- Visual acuity of 6/18 in the left eye and 6/12 in the right eye. 
Relative Afferent Pupillary Defect  + in LE 
Color vision and field of vision are normal. 
Oculomotor, Trigeminal, and Abducent nerves- The patient has restricted movement in the 
Left eye in abduction (Lateral Rectus), Depression, and Intorsion (Superior Oblique). 
Ocular position-Esotropia of the left eye. 
Image showing Esotropia of the left Eye 
Aperture, Pupil size, and accommodation are unremarkable. 
No nystagmus or Ptosis. 
Trigeminal nerve- Loss of sensation over the V1 branch. 
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Other cranial nerves- Intact. 
Motor system: Normal bulk, tone normal in both upper and lower limbs, Power 5/5 in both 
upper and lower limbs, plantars-flexor bilaterally. 
Sensory system: unremarkable. 
Cerebellar signs and meningeal signs absent. 
Peripheral nerve examination-Normal. 
Fundoscopy: Normal fundus. No papilloedema. 
Cardiovascular System: S1 S2 + 
Respiratory System:B/L Normal vesicular breath sounds 
Per Abdomen-Soft, non-tender, no organomegaly 
 
Investigations 
Hemoglobin-12.8 g/dl 
Total leucocyte Count-8900 cells/cumm 
Platelet count-3.86 lakh/cumm 
T3-1.12 ng/ml 
T4-9.0 mcg/ml 
TSH-1.12 mcIU/ml 
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S.G and P: “Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROM
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PT-14.5 sec 
INR-1.13 
Blood urea-23 mg/dl 
Serum creatinine-0.8 mg/dl 
CSF Fluid analysis- 
:cells- 10(lymphocytes) 
: Glucose-71 mg/dL 
: Protein-122.6 mg/dL 
: Chloride-116 mmol/L 
:Gram stain-Nil 
:KOH-No fungal elements 
:Acid Fast Bacilli not seen. 
MRI BRAIN(plain and contrast): Enhancing soft tissue lesion in left cavernous sinus with 
extension and mild compression and medial displacement of the optic nerve at the orbital 
apex. 
Mildly hyperintense left lateral rectus muscle. 
Bulky left lacrimal gland- Tolosa Hunt Syndrome to be considered. 
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MRI Brain – Arrow shows enhancing soft tissue lesion in Left Cavernous Sinus 
 
Diagnosis 
TOLOSA-HUNT SYNDROME –ORBITAL APEX SYNDROME 
Treatment 
The patient was started on IV Dexamethasone and switched over to oral corticosteroids 
which is the mainstay of treatment. 
Treatment given: 
INPATIENT: INJ DEXAMETHASONE 4mg IV 1-1-1 for 5 days f/b 1-0-1 for 2 days 
OUTPATIENT: TAB DEXAMETHASONE(1mg/kg body wt) 40mg 1-0-0 for 1 week f/b 
30mg 1-0-0 for 1 week f/b 
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S.G and P: “Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROM
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20mg 1-0-0 f/b 
10mg 1-0-0 for 1 week then stopped. 
Usually, oral steroids are tapered over 4-6 weeks according to the steroid response of the 
particular patient. 
 
 
Discussion 
DEFINITION: It is a syndrome of painful ophthalmoplegia which is characterized by 
periorbital and/or hemicranial pain, palsy of the ocular motor nerves (III, IV, and VI) on the 
same side, loss of sensation along with the ophthalmic division of the V cranial nerve, 
occasionally the maxillary division due to chronic non-specific inflammation. 
Superior orbital fissure syndrome refers to symptom complex produced by the involvement 
of the III, IV, VI, and V1 cranial nerves. 
Orbital apex syndrome refers to the symptom complex produced by the involvement of 
structures passing through superior orbital fissure and optic canal, characterized by 
involvement of II, III, IV, VI, and V1 cranial nerves[1]. 
The incidence of Tolosa-Hunt syndrome is equal among both the sexes with a prevalence of 
1-2 cases per million.[2] 
CLINICAL FEATURES:[1] 
1. Pain-unilateral, periorbital, retro-orbital and/or hemi-cranial. 
2. Ophthalmoplegia, i.e, the involvement of the III, IV, VI cranial nerves with or without 
the involvement of the II cranial nerve on the same side. 
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3. Vision may or may not be affected. 
4. Ptosis may occur due to the involvement of III cranial nerve on the same side. 
5. Loss of sensation over the forehead and face may occur due to the involvement of the 
ophthalmic division, occasionally maxillary division of the V cranial nerve, on the 
same side. 
6. Uncommonly, patients may also have systemic features like nausea and vomiting, due 
to severe pain. 
DIAGNOSTIC CRITERIA( IHS CLASSIFICATION ICHD-3 BETA)[3] 
1.  Unilateral headache 
2. Including both of the following criteria: 
3. MRI or Biopsy showing the presence of granulomatous inflammation of the 
cavernous sinus, superior orbital fissure, or orbit. 
4. Ipsilateral palsy of one or more Occulomotor nerves(III, IV, VI) 
3. Headache which is not explained by any other etiology. 
Although according to the diagnostic criteria Tolosa Hunt syndrome is unilateral 
ophthalmoplegia, there have been few reported cases of bilateral ophthalmoplegia, evidenced 
by the fact there was a response to steroids and the symptoms not explained by any other 
conditions[4]. 
DIFFERENTIAL DIAGNOSIS FOR PAINFUL OPHTHALMOPLEGIA:[1] 
1. Inflammatory causes: Rhinocerebral mucormycosis, bacterial sinusitis, orbital 
cellulitis, Herpes Zoster, Mycobacterial tuberculosis, Sarcoidosis, Tolosa-Hunt 
Syndrome, Wegener’s Granulomatosis. 
2. Vascular causes: Carotid-cavernous fistula, Carotid-cavernous thrombosis, carotid 
artery aneurysm. 
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S.G and P: “Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROM
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3. Neoplastic causes: Meningioma, Pituitary adenoma, Nasopharyngeal carcinoma, 
Craniopharyngioma, Neurofibroma. 
4. Trauma 
Rhinocerebral mucormycosis is the most frequent cause for cavernous sinus syndrome, which 
has to be ruled out in patients with Diabetes, transplantation, prolonged neutropenia, or 
malignancy, with complete ENT examination and MRI brain[5]. 
INVESTIGATIONS:[1,5] 
1. Hematology: Complete hemogram, Liver and Renal function tests, Blood glucose, 
Erythrocyte Sedimentation Rate, C-Reactive Protein, Hemoglobin A1c, Treponemal 
tests, Antinuclear Antibody Profile,  protein electrophoresis, Angiotensin-Converting 
Enzyme levels. 
2. Cerebrospinal fluid:  pressure, Cell count, Differential count, Microscopy, Glucose, 
Protein, Chloride Culture, Cytology, Angiotensin-converting enzyme, ADA. 
3. Neurological studies: Magnetic Resonance Imaging,  Computed Tomography, 
Cerebral Angiography 
When MRI is being used to detect the presence of granulomatous tissue in the orbital region, 
the T1 sequence can be used with slice thickness being as low as 2mm, as the granulomas are 
not larger than 1 or 2mm.[4] 
4. Biopsy:  Cavernous Sinus 
TREATMENT: The mainstay of treatment is glucocorticoids.  Oral prednisone (60mg daily) 
is given for 2 weeks and gradually tapered over a month or longer if the pain is still 
persistent[5]. 
There is a dramatic response to the steroids in terms of the symptoms, the pain is relieved 
within 24-72 hours, cranial nerve palsies improve gradually over 2-8 weeks. 
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Some patients may also require immunosuppressive drugs such as Azathioprine, 
Methotrexate, Mycophenolate mofetil, Cyclosporine, Infliximab for either suppression of the 
disease process or to avoid the long term effects of steroid therapy. 
In patients with contraindications to Steroid therapy, Radiotherapy can be used as the first 
line of management after a biopsy-proven diagnosis of Tolosa-Hunt syndrome. 
Relapses can occur in 40-50% of the patients and are more common in younger patients. The 
role of steroids in relapse is unclear[3]. 
References 
1. Kline L, Hoyt W.  The Tolosa-Hunt syndrome. Journal of Neurology, Neurosurgery 
& Psychiatry. 2001. 
2. M.E. Ceylan, A. Evrensel, C.O.Noyan, A.Donmez. Tolosa-Hunt syndrome and 
comorbidity of an obsessive-compulsive disorder and aortic aneurysm.BMJ Case Rep. 
2016. 
3. Chaitanya Amrutkar , Erik V. Burton. Tolosa-Hunt syndrome. August 10, 2020. 
4. I. Kastirr, P. Kamusella, R. Andresen, Bilateral painful ophthalmoplegia: a case of 
assumed Tolosa-Hunt syndrome. J. Clin. Diagn. Res. 10(3), TD16–TD17 .2016 
5. Dan L Longo, Dennis L Kasper, J. Larry Jameson, Anthony S. Fauci, Stephen L. 
Hauser, Joseph Loscalzo. Harrison’s Principles of Internal Medicine. 18th edition. 
New York: Mc Graw Hill; 2012. 
 
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S.G and P: “Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROM
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“Hunting” a case of External Ophthalmoplegia: TOLOSA-HUNT SYNDROME

S, Chandran

Digital Journal of Clinical Medicine 
Volume 2 Issue 2 Article 7 
1-1-2020 
A Case of Recurrent Pregnancy Loss due to Bicornuate Uterus 
Chandran S 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
S, Chandran (2020) "A Case of Recurrent Pregnancy Loss due to Bicornuate Uterus," Digital Journal of 
Clinical Medicine: Vol. 2: Iss. 2, Article 7. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of Recurrent Pregnancy Loss due to Bicornuate Uterus 
  
Chandran S, 7TH term, JSS Medical College,JSS AHER,Mysuru  
 
Clinical History 
30 year old G10 P4 L2 A5 D2 came with h/o 1.5 months of amenorrhoea with c/o bleeding PV since 2 
weeks a/wpain,c/o fatigue since 2 days. 
History of present pregnancy : 1st trimester – conceived spontaneously, pregnancy detected by UPT 
1 week back, confirmed by USG. 
 
Obstretic History 
G10 P4 L2 A5 D2 
1st – concieved spontaneously, breech delivery, male died at 22 days. Cause of death – jaundice 
2nd- conceived spontaneously, spontaneous abortion at 2 months, D&C done 
3rd – conceived spontaneously, spontaneous abortion at 2.5 months 
4th – conceived spontaneously, spontaneous abortion at 1.5 months 
5th – conceived spontaneously, spontaneous abortion at 3 months 
6th – conceived spontaneously, cervical encerclage at 4th month, FTND, female baby died at 2 years. 
Cause of death – Tuberculosis 
7th – conceived spontaneously, FTND, female baby, 9 years of age, currently active and healthy 
8th – concieved spontaneously, FTND, female baby, 8 years of age, currently active and healthy. 
9th – concieved spontaneously, consumption of MTP pills at 1.5 months, complete abortion. 
10th – conceived spontaneously, present one. 
Menstrual history: 
LMP – 9/3/19 
EDD – 16/12/19 
POG – 6 weeks 2 days 
Past cycles – 3-5/30, regular, moderate flow, No pain , No clots. 
H/o of Laproscopic sterilization done in 2011 and 2015 
 
 
 
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Examination: 
GENERAL PHYSICAL EXAMINATION: 
Pulse – 84 bpm 
BP – 130/80 mm Hg 
Pallor absent 
SYSTEMIC EXAMINATION : 
CVS – S1, S2 heard. No murmurs 
RS – B/L normal vesicular breath sounds heard. No added sounds 
P/A – Soft, non tender. No organomegaly 
P/S – No discharge, cervix healthy 
P/V – uterus bulky, corresponds to 8 weeks size. 
Investigations: 
Hb – 12.4gm/dl (12-15 gm/dl) 
TLC – 11410 cells/cumm (4000 – 11000 cells/cumm) 
DC: Neutrophils – 59.1 
Lymphocytes – 34.9 
Eosinophils – 1.6 
Monocytes – 4.1 
Basophils – 0.3 
PCV – 38.9 (36-46%) 
Rbc count – 5.08 million/cumm (3.8-4.8 million/cumm)  
Diagnosis: 
1. Chromosomal abnormality 
2. Inherited thrombophilias 
3. Anti -phospholipid antibody syndrome 
4. Poorly controlled diabetes 
5. Thyroid autoantibodies 
6. Luteal phase defect 
7. Polycystic ovarian syndrome 
Diagnosis: 
30 Year old Gravida 10 Para 4 Living 2 Abortion 5 Death 2 with 6 weeks 2 days of gestation 
with BicornuateUnicollis Uterus with implantation in the left horn. 
 
 
 
 
 
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Treatment: 
Procedure: 
MTP with Laproscopic bilateral salpingectomy under GA. 
 
Laproscopic findings: 
BicornateUnicollis uterus noted 
Right hydrosalpinx noted 
Fallope rings of old tubectomy present on the right tube 
Left tube not tubectomized 
Bilateral salpingectomy done 
 
Per-operative findings: 
Products of conception present in the left horn 
6 weeks size uterus noted 
Products sent for HPE. 
 
Discussion: 
Congenital uterine anomalies result from the abnormal formation, fusion, or resorption of Müllerian 
duct during fetal life. 
They are present in, 2–8% of infertile women, and 5–30% of women with a history of miscarriage(1). 
Premature deliveries (29%), spontaneous first-trimester abortions (24%), ectopic pregnancies (3%), 
abnormal fetal presentations (23%) and a high cesarean section rate (27.5%) occurred in those 
patients. 
In 30% of the patients, cervical incompetence was diagnosed. Improved obstetric outcomes occurred 
in patients treated with cervical cerclage(5). 
Although uterine anomalies are associated with adverse reproductive outcomes, healthy reproductive 
outcomes are possible. 
Females with obstructive uterine anomalies tend to present during adolescence due to pelvic pain or 
dysmenorrhea, and those with non obstructive uterine anomalies may not be identified until 
evaluation of pregnancy loss, an obstetric complication, or infertility is initiated. 
Imaging modalities to evaluate congenital uterine anomalies include two-dimensional ultrasonography 
(2DUS), three-dimensional ultrasonography (3DUS), hysterosalpingography, saline infusion 
ultrasonography, and magnetic resonance imaging (MRI). 
As 3DUS is increasingly utilized in pelvic imaging, this modality is proving to be highly accurate in 
diagnosing uterine anomalies and may be equivalent to MRI(2). 
Widely diverging horns seen on HSG may suggest a bicornuate uterus and an intercornual angle 
greater than 105 degrees suggests bicornuate uterus, whereas one less than 75 degrees indicates a 
septate uterus. However, MRI may be necessary to define fundal contour. 
With this, an intrafundal downward cleft measuring greater than or equal to 1 cm is indicative of 
bicornuate uterus, whereas a cleft depth < 1 cm indicates a septate uterus(9) 
Over the years, surgical treatments have been offered to women diagnosed with congenital uterine 
anomalies. 
Abdominal metroplasty is associated with significant morbidities, such as prolonged hospital stay, 
long post-op recovery, intra-abdominal adhesions, uterine rupture in subsequent pregnancies etc.(3) 
Strassman metroplasty provides an important decrease in the percentage of fetal loss (8-12%) 
compared to patients without surgical treatment (70-96%).(7) It is a unification procedure performed 
to correct the two smaller uterine cavities into a more spacious single cavity. Improved reproductive 
performance was reported after unification metroplasty. Laparoscopic route can be adopted for this 
procedure with all the advantages of minimally invasive surgery. The laparoscopic route provides 
better magnification, lower tissue drying, reduced infections, lesser adhesions, shorter hospital stay, 
3
S: A Case of Recurrent Pregnancy Loss due to Bicornuate Uterus
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and quicker recovery. (6) The actual benefit of metroplasty for a bicornuate uterus, however, has not 
been tested in a controlled clinical trial and metroplasty for now should be reserved for women in 
whom recurrent pregnancy loss occurs with no other identifiable cause(8). 
According to the CREST study, the 10-year failure rate is 18.5 per 1000 procedures.The pregnancy 
rates were highest following laparoscopic Hulka clip sterilization and lowest following monopolar 
coagulation and postpartum salpingectomy (4) 
 
USG abdomen of bicornuate uterus 
https://radiopaedia.org/articles/bicornuate-uterus 
 
HSG of bicornuate uterus 
https://radiopaedia.org/cases/bicornuate-vs-septate-uterus?lang=us 
References: 
1. Chan, Yee Yin (2019) Study to evaluate the prevalence, importance, and treatment of women 
with congenital uterine anomalies. PhD thesis, University of Nottingham. 
2. Rackow B.W. (2019) Congenital Uterine Anomalies. In: Stadtmauer L., Tur-Kaspa I. (eds) 
Ultrasound Imaging in Reproductive Medicine. Springer, Cham 
3. G. Zlopaša,S. Škrablin ,D. Kalafatić ,V. Banović ,J. Lešin.Uterine anomalies and pregnancy 
outcome following resectoscope metroplasty. Volume 98. International journal of 
gynaecology and obstetrics; 2007. 
4. Gossman W, Canela CD, Nama N. Tubal Sterilization StatPearls [Internet]. Treasure Island 
(FL): StatPearls Publishing; 2020 Jan 
5. Golan A,Langer R, Neuman M, Wexler S, Segev E, David MF,Obstetric outcome in women 
with congenital uterine malformations, Journal of reproductive medicine, 1992 
Mar;37(3):233-6. 
6. SDS Karthik, Alka Kriplani, Reeta Mahey,Garima Kachhawa, Successful reproductive 
outcome after Laparosopic strassman metroplasty, Journal of Human reproductive sciences, 
2017 Jul-Sep; 10(3): 231–234. 
7. R. Tomasz, M. Marta, and B. Aleksandra, “Clinical effectiveness of Strassman operation in 
the treatment of bicornuate uterus,” Ginekologia Polska, vol. 80, no. 2, pp. 88–92, 2009. 
8. M. Sugiura-Ogasawara, B. L. Lin, K. Aoki et al., “Does surgery improve live birth rates in 
patients with recurrent miscarriage caused by uterine anomalies?” Journal of Obstetrics & 
Gynaecology, vol. 35, no. 2, pp. 155–158, 2015. 
9. K. L. Reuter, D. C. Daly, and S. M. Cohen, “Septate versus bicornuate uteri: Errors in 
imaging diagnosis,” Radiology, vol. 172, no. 3, pp. 749–752, 1989. 
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A Case of Recurrent Pregnancy Loss due to Bicornuate Uterus

A, Nair

R, Prasad

S, Dr. Ravikumar

Kumar, Dr. Prasanna

Digital Journal of Clinical Medicine 
Volume 2 Issue 2 Article 6 
1-1-2020 
A Case of Megaloblastic Anemia With Suspected Gilbert 
Syndrome 
Nair A 
JSS AHER 
Prasad R 
JSS AHER 
Dr. Ravikumar S 
JSS AHER 
Dr. Prasanna Kumar 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
A, Nair; R, Prasad; S, Dr. Ravikumar; and Kumar, Dr. Prasanna (2020) "A Case of Megaloblastic Anemia 
With Suspected Gilbert Syndrome," Digital Journal of Clinical Medicine: Vol. 2: Iss. 2, Article 6. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case of Megaloblastic Anemia With Suspected Gilbert Syndrome 
 
Nair A, Prasad R, MBBS 
Dr.Ravikumar, Dr.Prasanna Kumar, Dr.Sneha Department of Medicine, JSS Hospital, JSSAHER 
Clinical history: 
A 27 year old male patient came with complaints of generalized weakness since 15 days associated 
with nausea and reduced appetite. 
He also complained of fever, low grade, intermittent in nature with no diurnal variation. 
No history of loose stools. 
No history of joint pains or rashes. 
k/c/o GILBERT SYNDROME- diagnosed two years ago (details not available) 
Examination: 
GENERAL PHYSICAL EXAMINATION: 
Afebrile. 
Pallor and icterus present. 
No generalised lymphadenopathy noted. 
PER ABDOMEN: 
Inspection: 
Shape of abdomen: normal 
Umbilicus central. 
No distention visible 
Palpation : 
No local rise of temperature or tenderness noted. 
Spleen is palpable 3cm below the left costal margin. 
Percussion: Traube space is obliterated-dullness noted. 
No Signs of free fluid. 
Auscultation. Normal bowel sounds heard. 
CVS: S1, S2 heard. No murmurs. 
RS: B/L NVBS heard. No added sounds. 
CNS: Within normal limits 
Investigations: 
BLOOD INVESTIGATIONS: 
Hb-5.5gm% 
TLC-3670 cells/cumm 
N-47.9 
L-43.9 
RBC count-1.47million/cumm 
MCV– 109fl 
MCH -37.3 pg 
MCHC -34.3 g/dl 
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Platelet count-44,000/cumm 
Direct coombs test-negative 
Retic count-6% 
Vit B12-1254pg/ml (190-950pg/ml 
Folic acid-1.2ng/ml(2-20ng/ml) 
LDH-1535U/L (125-220U/L) 
PBS picture: 
Pancytopenia with anisopoikilocytosis, fragmented RBCs, basophilic stippling, tear drops cells noted. 
9/100WBC, polychromatophils 
Blood picture of megaloblastic anemia-macroovalocytes with 
hypersegmented neutophils. 
 
Ref: http://doi.org/10.7939/R36970D1B 
 
LIVER FUNCTION TEST: 
Total bilirubin -3.53mg/dl 
Direct bilirubin-0.46mg/dl 
 
Diagnosis: 
▪ Pancytopenia due to Megaloblastic anemia secondary to nutritional deficiency 
▪ Gilbert Syndrome ?? 
Treatment: 
▪ Patient was treated with 1500 micrograms of Vitamin B12 injection and 5 mg of folic acid 
tablets. 
▪ Two pint PRBC transfusion was given after which his Hb improved from 5.5gm% to 
9.3gm%. 
▪ Patient was discharged with the advice to continue B12 and Folic acid. 
Discussion:  
Megaloblastic anemia results from the deficiency of vitamin B12, or folic acid or from disturbances in 
folic acid metabolism.Folate is an important substrate of and vitamin B12 an important co factor for 
the generation of essential amino acid methionine from homocyteine.Deficiency of vitamin B12 or 
folate will therefore produce high plasma levels of homocyteine and impair DNA synthesis. 1 
The end result is cells with arrested nuclear maturation but normal cytoplasmic development-so called 
nucleocytoplasmic asynchrony.1 
High proliferation rate of bone marrow results in striking changes in hematopoietic system in 
megaloblastic anemia.Cells become arrested in development and die within the marrow,this 
ineffective erythropoiesis results in an expanded hypercellular bone marrow.1 
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Macrocytic anemia with increased mean corpuscular volume (MCV), defined as more than 100 fL, is 
the hallmark of megaloblastic anemia, but leukopenia and thrombocytopenia are also frequently 
present.2 Megaloblastic anemia is the commonest cause for pancytopenia 
Since Megaloblasts are prone for hemolysis, LDH is increased. This could be the cause for indirect 
hyperbilirubinaemia. There is every possibility that the patient could have been wrongly diagnosed to 
be having Gilbert Syndrome. 
Gilbert syndrome is an autosomal dominant trait caused by mutation in the promoter region of UDP-
glucuronyl transferase enzyme,which leads to reduced enzyme expression.This results in decreased 
conjugation of bilirubin,which accumulates as unconjugated bilirubin in the blood.1 
Typical presentation is with isolated elevation of bilirubin,typically,although not exclusively,in the 
setting of physical stress or illness.1 
The only significant laboratory abnormality in patients with Gilbert syndrome is increased 
unconjugated bilirubin levels, and they are usually below 3 mg/dL with less than 20% of the bilirubin 
levels being conjugated. When associated with other pathological conditions which increase 
hemolysis, the level can be higher, but even then it is usually below 6 mg/dL.3 
References: 
1. Walker B, R.Colledge N, H Ralston S, D Penman I. Davidson’s principles and practices of 
medicine. 22nd ed. Churchill Livingstone; 2014. 
2. Socha D, DeSouza S, Flagg A, Sekeres M, Rogers H. Severe megaloblastic anemia: Vitamin 
deficiency and other causes. Cleveland Clinic Journal of Medicine. 2020;87(3):153-164. 
3. Viveksandeep T, Savio J. Gilbert syndrome. [Internet]. 2020 [cited 7 March 2020];. Available 
from: https://www.ncbi.nlm.nih.gov/ 
 
 
3
A et al.: A Case of Megaloblastic Anemia With Suspected Gilbert Syndrome
Published by Research Connect, 2020


A Case of Megaloblastic Anemia With Suspected Gilbert Syndrome

M, Dr Kruthi

Prasad S, Dr Rajendra

Digital Journal of Clinical Medicine 
Volume 2 Issue 5 Article 10 
1-1-2020 
A Case Of Tenofovir Induced Osteopenia 
Dr Kruthi M 
JSS AHER 
Dr Rajendra Prasad S 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
M, Dr Kruthi and Prasad S, Dr Rajendra (2020) "A Case Of Tenofovir Induced Osteopenia," Digital Journal 
of Clinical Medicine: Vol. 2: Iss. 5, Article 10. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case Of Tenofovir Induced Osteopenia 
Dr Kruthi, 7th term MBBS 
Dr Rajendra Prasad S, Associate Professor, General Medicine, JSS Medical College, JSS 
AHER 
Clinical history 
A 33-Year-old female patient who is a known case of retroviral disease, diagnosed in 2013 
was on TLE regime (TENEFOVIR 300MG, LAMIVUDINE 300MG, EFAVIRENZ 
600MG), now complaints of generalized bone pain for 2-3 months. 
No history of fever, cough, any localized swelling, weight loss, rashes. Her menstrual cycles 
are regular with moderate amount of flow. 
Past history includes TB pleural effusion, TB meningitis, Paradoxical TB IRIS, bacterial 
pneumonia for which she underwent treatment.         
Not a known case of diabetes mellitus, hypertension, cardiac disease, thyroid disorder, 
asthma, epilepsy. 
Non-smoker, non-alcoholic. 
Examination 
GPE: Middle aged female patient moderately built and nourished, well oriented to time, 
place, person.  Is alert, conscious and cooperative. 
Pulse: 80 bpm 
Blood pressure: 130/80 mm hg 
Temperature: 97.4* F 
Respiratory rate: 18 cpm 
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M and Prasad S: A Case Of Tenofovir Induced Osteopenia
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No pallor, icterus, cyanosis, clubbing, edema, lymphadenopathy. 
SYSTEMIC EXAMINATION: RS:  B/L NVBS,No added sounds 
CVS: S1, S2 heard. no murmurs 
P/A: Soft, non-tender. Mild hepatomegaly +. Normal bowel sounds. CNS: No focal 
neurological deficits.        
Investigations 
Hb: 10.6 gm/dl 
TLC:  7000 cells/mm3 
Urea: 18 mg/dl 
Creatinine: 0.8 mg/dl 
SGOT: 22 IU/L 
SGPT: 6 IU/L 
Viral load: < 20 copies / milliliter 
CD4 count: 600 cell/mm3 
Bone Mineral Density report is suggestive of Osteopenia 
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BMD Scan 
 
Diagnosis 
TENEFOVIR INDUCED OSTEOPENIA 
 
Treatment 
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M and Prasad S: A Case Of Tenofovir Induced Osteopenia
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Tenefovir was discontinued and her ART regimen was 
substituted  to ABACAVIR 600MG, LAMIVUDINE 300MG, EFAVIRENZ 600MG once 
daily. 
Discussion: 
Tenofovir is a monophosphate nucleotide which is active against HBV and HIV. It acts by 
inhibiting HIV reverse transcriptase enzyme. Due to its low oral absorption, it is used as 
tenofovir disoproxil ester prodrug. It has relatively fewer side effects which include nausea, 
abdominal discomfort; slight increase in serum creatinine, chronic renal disease.(1) 
Lately it has been shown that long term usage of tenofovir is associated with loss of bone 
mineral density. Studies have shown that there is approximately 1-3% greater bone mineral 
density loss with Tenefovir containing regimen.(2) 
Osteopenia and fractures are associated with HIV infection itself but tenefovir also leads to 
increased bone catabolism markers and decreased bone mineral density.(3) 
Also, a note on IMMUNE RECONSTITUTION INFLAMMATORY SYNDROME (IRIS)– 
It is the paradoxical worsening of preexisting opportunistic infection following initiation of 
antiretro viral therapy. 
IRIS related to known pre-existing infection or neoplasm is known as paradoxical IRIS, while 
IRIS associated with previously undiagnosed condition is known as unmasking IRIS. (4) 
References 
1. K.D TRIPATHI, 8TH EDITION, TEXTBOOK OF PHARMACOLOGY. 
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Digital Journal of Clinical Medicine, Vol. 2 [2020], Iss. 5, Art. 10
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2.Grant PM, Cotter AG. Tenofovir and bone health. Current opinion in HIV and AIDS. 2016 
May;11(3):326. 
3.Conesa‐Buendía FM, Llamas‐Granda P, Larrañaga‐Vera A, Wilder T, Largo R, Herrero‐
Beaumont G, Cronstein B, Mediero A. Tenofovir causes bone loss via decreased bone 
formation and increased bone Resorption, which can be counteracted by dipyridamole in 
mice. Journal of Bone and Mineral Research. 2019 May;34(5):923-38. 
4. HARRISON`S PRINCIPLES OF INTERNAL MEDICINE, 20TH EDITION.   
 
 
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A Case Of Tenofovir Induced Osteopenia

Sinha, Nimisha

Anurika, Sakshi

Prerana, Dr. Anu

Digital Journal of Clinical Medicine 
Volume 2 Issue 3 Article 6 
1-1-2020 
Uterine Prolapse 
Nimisha Sinha 
JSS AHER 
Sakshi Anurika 
JSS AHER 
Dr. Anu Prerana 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Sinha, Nimisha; Anurika, Sakshi; and Prerana, Dr. Anu (2020) "Uterine Prolapse," Digital Journal of Clinical 
Medicine: Vol. 2: Iss. 3, Article 6. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Uterine Prolapse 
 Nimisha Sinha, Sakshi Anurika, Dr. Anu Prerana  
Clinical History 
A 55-year-old female presented to the   OBG department with complaints of pain in lower 
abdomen, the flanks, dysuria, urinary incontinence and constipation since one month.  
She felt a mass protruding per vagina a year ago, but it didn’t interfere with her daily activities.  
She has a past history of three caesarean deliveries. 
Obstetric Score of the patient is G3P3A0L3. 
Menstrual history is normal. 
She does not have a history of any connective tissue disorder, hypertension, diabetes mellitus, 
cardiac, respiratory and thyroid disorders. 
Examination and Investigation 
General Physical Examination  
The female patient was conscious, alert, cooperative and well oriented to time, place and person. 
She was moderately built and well nourished. 
No pallor, icterus, cyanosis, clubbing, lymphadenopathy or edema. 
Blood pressure- 108/82 mm of Hg 
Pulse-80 bpm 
Systemic Examination  
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CVS – S1, S2 heard. No murmur. 
RS – B/L normal. 
Abdomen – Soft bowel sounds present. 
P/V Examination – Protrusion of globular mass outside vaginal introitus. 
 
Haematological investigation: 
Total RBC count– 4millions/cu mm 
Total WBC count– 7500/cu mm 
Platelet count– 1.3lakhs/ cu mm 
HCT– 33.4% 
Hb– 10.6g/dl  
BT– 1min 55sec 
CT– 4min10sec 
PT– 13sec 
Card HIV– negative 
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HCV antibody test-negative 
Card test HBs Ag– Non- reactive 
Thyroid Profile 
T3 – 1.14mg/ml 
T4 – 6.8 micrograms/dl 
TSH – 2.41 pIU/ml 
PAP smear report: 
Suggestive of atrophic smear. No dysplastic cells seen. 
USG scan of abdomen and pelvis 
Liver, GB, pancreas, spleen, kidneys and UB are normal. 
Both ovaries atrophied and no ovarian/adnexal mass is seen. 
Uterus- Prolapsed uterus (size- 86×31×50mm) with hypertrophied cervix. 
Final Diagnosis 
Procidentia/ Uterine prolapse Grade 4 
Discussion 
Uterine prolapse is the descent of uterus per vagina due to loss of anatomical support of the 
uterus by pelvic floor muscles and uterosacral, round, broad and cardinal ligaments. 
Uterine prolapse can be categorized as incomplete and complete. 
Incomplete uterine prolapse: Uterus partially displaced into vagina but doesn’t protrude out. 
Complete uterine prolapse: Portion of uterus protrudes outside vagina. 
The condition is graded by the level of descent of uterus into vagina: 
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Grade 1- Descent of uterus to upper vagina 
Grade 2- Descent of uterus to introitus of vagina. 
Grade 3- Descent of cervix outside introitus of vagina. 
Grade 4- Descent of cervix and uterus outside vagina. 
Signs and symptoms include uterine protrusion from vaginal opening, backache, pelvic 
heaviness and pulling, sense of ‘dragging’ pain in the groin, dysuria, urinary incontinence, 
retention of urine in bladder, susceptibility to UTIs, vaginal bleeding or discharge, abdominal 
cramping, constipation and ulceration of exposed tissue. 
Symptoms are often exacerbated by chronic coughing, straining or prolonged standing. 
The most probable causes of uterine prolapse are obesity, genetic predisposition, excessive 
straining during bowel movements, multiple deliveries, trauma during childbirth per vagina, 
weakness of pelvic supports due to aging, decreased estrogen levels and disorders of connective 
tissue. 
Treatment options include hormone replacement therapy, insertion of vaginal pessary, exercises 
to strengthen pelvic muscles and in severe cases, surgery. 
Though uterine prolapse is often asymptomatic but patients should approach a doctor without 
any hesitation as early as possible to prevent progress to manifestation of urological symptoms. 
Acknowledgements: None  
References  
1. Young JB, Selby PL, Peacock M, Brownjohn AM. Uterine Prolapse And Urinary Tract 
Obstruction.Br Med J.1984; 289(6436):41; 2 
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DOI: –
2. Sampathkumari S et al. A Rare Case of Prolapse Uterus. Indian Journal Of Clinical Uterus 2013; 
24(6):566-7. 
3. Karateke A, Gurbuz K, Kabaca C, Mengulluoglu M. Sacrocervicopexy And Combined 
Operations Involving Cases Of Total Uterine Prolapse 2003;13:164-68 
4. Hove MC et al. The Prevalence Of Pelvic Organ Prolapse Symptoms And Signs And Their 
Relation With Bladder amd Bowel Disorders In A General Female Population. Int Urogynecol J 
2009;20:1037-45 
5. Smith L. What do you need to know about uterine prolapse.2017.Available from 
www.medicalnewstoday.com 
6. Doshani A et al. Uterine Prolapse.2007. Available from 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2034734 
 
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Uterine Prolapse

Dadlani, Diksha

Digital Journal of Clinical Medicine 
Volume 2 Issue 1 Article 6 
1-1-2020 
Tubular Adenoma of Breast 
Diksha Dadlani 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Dadlani, Diksha (2020) "Tubular Adenoma of Breast," Digital Journal of Clinical Medicine: Vol. 2: Iss. 1, 
Article 6. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Tubular Adenoma of Breast 
Diksha Dadlani, Mohali, Punjab  
CLINICAL HISTORY: 
17-year-old female presented to the surgery department of Government Medical College and 
Rajendra Hospital, Patiala, with a gradually enlarging palpable, asymptomatic mass in the 
middle outer portion of the left breast. She had first noticed the mass 2 years ago and had 
then undergone a sonography at another institution that revealed a well circumscribed, 
homogenous, hypoechoic mass measuring approximately 2.2 x 2cm at that time. She had no 
history of bronchial asthma, rheumatoid arthritis, diabetes, hypertension, hypothyroidism, any 
bleeding disorder or any other previous surgery. She also had a negative family history of 
breast or ovarian malignancies. The female had undergone menarche at the age of 14 and her 
menstrual cycles were regular. 
 
EXAMINATION AND INVESTIGATIONS: 
General and Systemic Examination- Normal. 
Local physical examination: 
• Painless, non-tender, mobile, well circumscribed mass was palpated in the middle 
outer portion of left breast at 3 0’ clock position. 
• Skin overlying the swelling was normal and no nipple discharge or inflammatory 
changes were present. 
• No palpable supraclavicular or axillary lymph nodes. 
 
Ultrasound: Well defined hypoechoic mass in the left breast with imaging features suggestive 
of non-calcified fibroadenoma. 
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FNAC: Cohesive clusters of dual population of ductal epithelial cells and myoepithelial cells 
along with naked, bipolar nuclei in the background – s/o fibroadenoma. 
Histopathological examination of the surgically excised tumor: Closely packed small tubules 
lined with a bilayer of epithelial cells and myoepithelial cells were seen. Scanty connective 
tissue stroma was seen between the tubules. The mass was thus diagnosed as tubular breast 
adenoma. 
 
FINAL DIAGNOSIS: 
Clinico-radiological differentials for tubular adenoma includes Fibroadenoma. 
Histologically, the differential diagnosis of tubular adenoma includes fibroadenoma, ductal 
carcinoma, microglandular adenosis, sclerosing adenosis, phyllodes tumour and tubular 
carcinoma 
 
DISCUSSION: 
Due to the history of progressive enlargement of the lump over the past two years, a surgical 
excision was carried out and a well circumscribed oval mass was resected. 
Macroscopically, the excised tumour measuring 6×5.5×3 cm presented as a solid, yellowish-
white elastic nodule with the surface showing slit-like areas, resembling a fibroadenoma. The 
patient had an 
uncomplicated postoperative course and she is doing well after 6 months of surgery. 
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▪  
▪  
 
Tubular adenoma is a rare benign neoplasm seen predominantly in women of reproductive 
age group, occurring rarely in postmenopausal women [1,8]. It presents as a painless, freely 
mobile, well-circumscribed mass with size rarely exceeding 5cm [3,10]. However, cases of 
giant tubular adenomas measuring over 14cm have also been reported[11,12]. It can 
potentially be confused with fibroadenoma due to the high degree of similarity in their 
clinical, radiological and cytological characteristics, thus making preoperative diagnosis 
extremely difficult [ 3,6]. Surgical excision or biopsy followed by histopathological 
examination is necessary to obtain a definitive diagnosis[3,6]. Immunohistochemical analysis 
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Dadlani: Tubular Adenoma of Breast
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by myoepithelial cells markers, combined with stromal markers, allows to rule out the 
various differential diagnoses, either malignant or benign tumors[3,7,13]. Although it is not 
known to be associated with the risk of malignant transformation, a few cases of adenoma 
associated with carcinoma have been reported[14,15]. However, a clear cut histological 
demarcation between the two lesions was present in all the reported case 
 
REFERENCES:  
1. Salemis. Tubular Adenoma of the Breast: A Rare Presentation and Review of the Literature. 
2019. 
2. 2.Hanby A, walker C. Tavassoli FA, Devilee P: Pathology and Genetics: Tumours of the 
Breast and Female Genital Organs. WHO Classification of Tumours series – volume IV. 
Lyon, France: IARC Press. Breast Cancer Research. 2004;6(3). 
3. Rare Breast Lesions: Correlation of Imaging and Histologic Features with WHO 
Classification | RadioGraphics [Internet]. Pubs.rsna.org. 2019 [cited 28 December 2019]. 
Available from: https://pubs.rsna.org/doi/full/10.1148/rg.285075743 
4. Sanjay Sengupta A. Evaluation of Clinico-Radio-Pathological Features of Tubular Adenoma 
of Breast: a Study of Ten Cases with Histopathological Differential Diagnosis [Internet]. 
PubMed Central (PMC). 2019 [cited 27 December 2019]. Available from: 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539785/ 
5. Tavassoli F, Devilee P. Pathology and genetics of tumours of the breast and female genitale 
organs. Lyon: IARC Press; 2003. 
6. Pal S, Biswas B, Phukan J, Sengupta S, Sinha A, Sinha R. Preoperative diagnosis of tubular 
adenoma of breast – 10 years of experience. 2019. 
7. Spruill L. Benign mimickers of malignant breast lesions. 2019. 
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8. Rovera F, Ferrari A, Carcano G, Dionigi G, Cinquepalmi L, Boni L et al. Tubular Adenoma 
of the Breast in an 84-Year-Old Woman: Report of a Case Simulating Breast Cancer. 2019. 
9. Soo MS e. Tubular adenomas of the breast: imaging findings with histologic correlation. – 
PubMed – NCBI [Internet]. Ncbi.nlm.nih.gov. 2019 [cited 27 December 2019]. Available 
from: https://www.ncbi.nlm.nih.gov/pubmed/10701621 
10. Tubular Adenoma of the Breast: A Clinicopathologic Study of a Series of 9 Cases – 
Boubacar Efared, Ibrahim S Sidibé, Souley Abdoulaziz, Nawal Hammas, Laila Chbani, 
Hinde El Fatemi, 2018 [Internet]. SAGE Journals. 2019 [cited 27 December 2019]. Available 
from: https://journals.sagepub.com/doi/full/10.1177/1179555718757499 
11. Huang Y, Zhang H, Zhou Q, Ling L, Wang S. Giant tubular adenoma of the accessory breast 
in the anterior chest wall occurred in a pregnant woman. 2019. 
12. Düşünceli F, Manukyan M, Midi A, Deveci U, Yener N. Giant Tubular Adenoma of the 
Breast: A Rare Entity. The Breast Journal. 2011;18(1):79-80. 
13. Maiorano E, Albrizio M. Tubular adenoma of the breast. 2019. 
14. Domoto H, Tsuda H, Miyakawa K, Shinoda A, Nanasawa T. Invasive ductal carcinoma 
associated with tubular adenoma of the breast. Pathology International. 2002;52(3):244-248. 
15. Saimura M, Anan K, Mitsuyama S, Ono M, Toyoshima S. Ductal carcinoma in situ arising in 
tubular adenoma of the breast. 2019 
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Tubular Adenoma of Breast

Suresh, DR Hitha

C P, DR Madhu

Digital Journal of Clinical Medicine 
Volume 2 Issue 5 Article 7 
1-1-2020 
A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis 
DR Hitha Suresh 
JSS AHER 
DR Madhu C P 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Suresh, DR Hitha and C P, DR Madhu (2020) "A Case Of Pancreatic Pseudocyst Following Acute 
Pancreatitis," Digital Journal of Clinical Medicine: Vol. 2: Iss. 5, Article 7. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis 
 
DR Hitha Suresh, 7th Term MBBS  
DR Madhu C P, Professor And Unit Chief, Dept Of General Surgery Jss Hospital Mysore, 
JSSAHER  
Clinical history 
A 35-year-old male presented with – 
▪ Complaints of pain abdomen, localized to the mid-upper abdomen and radiating to the 
back, for 2 days, aggravating on the consumption of food with no relieving factors. 
▪  Associated with vomiting, vomitus was non-bilious, non-blood tinged, and non-
projectile. 
▪ Complains of fever, moderate grade, and continuous for 1 day. 
▪ History of abdominal distension(+). 
▪ History of anorexia. 
▪ No history of loss of weight/jaundice/dyspepsia/clay-colored stools/high colored 
urine/bowel or bladder disturbances. 
        PAST HISTORY: 
▪ History of similar complaints one month back and was diagnosed as acute pancreatitis 
with cholelithiasis and was managed conservatively. 
▪ H/O chronic alcohol consumption before 13 years – (consumed whiskey 4-5 
times/week) 
 
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Suresh and C P: A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis
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Examination 
A middle-aged male patient moderately built and nourished, well oriented to time, place, and 
person, alert, conscious, and cooperative. 
No Pallor 
No Icterus 
No Cyanosis 
No Clubbing 
No generalized Lymphadenopathy 
No Edema 
Vitals: 
Pulse rate: 108 bpm 
BP: 130/82 mmHg 
RR: 20 CPM 
Temperature: febrile(100F) 
     Systemic Examination: 
1.PER ABDOMEN EXAMINATION 
INSPECTION: 
A spherical mass of ~10x8cm size present in the epigastric region does not move with 
respiration. 
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The skin over the abdomen normal, with no scars or sinuses. 
No visible pulsation or peristalsis, no dilated veins. 
Hernial orifices are normal. 
PALPATION: 
No local rise in temperature, 
   Tenderness present in the epigastric region+ 
   Spherical mass of 10x8cm palpate, localized in the epigastric region with well-defined 
margins and smooth surface tense and cystic inconsistency. 
   No Hepatosplenomegaly 
 PERCUSSION 
  Impaired resonance heard over the mass. 
  AUSCULTATION : 
  No bruits on auscultation. 
2.Cardio Vascular System: S1, S2 heard, no murmurs 
3.Respiratory System: Bilateral Normal vesicular breath sounds heard, no added sounds 
4.Central Nervous System:  No functional neurological disorder. 
 
Investigations 
Hb -14.8gm/dl 
 TLC-10380cells/cumm 
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Suresh and C P: A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis
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 DLC: 
 neutrophils-86.2 
 Lymphocytes10.4 
 Eosinophils-0.2 
 Monocytes-3.0 
 Basophils-0.2 
 PCV-42.4% 
 RBC count -4.99million/cumm 
 Random blood sugar-114mg/dl 
  Lipase – 116U/l 
 Amylase-613U/l 
 TLC:10380 cells/cumm 
 Platelet count -2.45 lakh/cumm 
 Albumin-3.5g/dl 
 Total proteins-5.8gm/dl 
 A.G ratio-1.5 
ast-13U/l 
Bilirubin direct-0.19mg/dl 
alt—12U/l  
ALP-85U/l 
MCV-85fl 
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Mchc-34.9gm/dl 
Serum Urea- 14mg/dl 
Serum Creatinine—0.69mg/dl 
Uric acid-3.7mg/dl 
Sodium-135mEq/L 
Chloride-97mEq/L 
CT ABDOMEN AND PELVIS (WITH AND WITHOUT CONTRAST) 
▪ Showed large well defined thick-walled peripherally enhancing cystic lesion 
measuring 10.8x13x1cm in the lesser sac -?pseudocyst. 
▪ Mild pancreatic and mesenteric fat stranding; minimal ascites -?acute pancreatitis. 
▪ Cholelithiasis with solitary distal CBD calculus. 
▪  Mild splenomegaly. 
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UGI ENDOSCOPY: 
Extrinsic impression over stomach (lesser curvature extending to distal body) -pseudocyst 
related 
Diagnosis 
Differential Diagnosis:  
* Pancreatic pseudocyst. 
* Gastric outlet obstruction due to peptic ulcer disease 
* Hydatid cyst 
*  Neoplasm of the pancreas. 
Diagnosis: 
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Suresh and C P: A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis
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PSEUDOCYST OF PANCREAS FOLLOWING ACUTE PANCREATITIS WITH 
CHOLELITHIASIS 
 
Treatment 
ENDOSCOPIC CYSTOGASTROSTOMY (a minimally invasive  method wherein EUS 
(endoscopic ultrasound)and fluoroscopy are used to identify the pseudocyst, and which helps 
in creating  a  fistula in between the cystic cavity and either the stomach/duodenum and thus 
helps in the drainage of the cyst .) 
 
Discussion 
Pseudocyst is a collection of amylase-rich fluid in a well-defined wall of fibrous granulation 
tissue, pseudocysts arise following acute pancreatitis and require about 4 weeks or more to 
form from the onset of acute pancreatitis (1) .pseudocyst account for 75%  of all pancreatic 
masses. Pseudocysts are classified into three types based on the underlying etiology of 
pancreatitis  They define three distinct types of pseudocysts  Type Ⅰ, or acute “post-necrotic” 
pseudocysts,(after an episode of acute pancreatitis with normal duct anatomy ). Type Ⅱ 
is  also termed as  post-necrotic pseudocysts(after an episode of acute on chronic pancreatitis 
with an abnormal pancreatic duct and often associated with a duct -pseudocyst 
communication)., 
Type Ⅲ is defined as “retention” pseudocysts, (after chronic pancreatitis with strictures and 
duct pseudocyst communication). (2) 
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Abdominal CT remains the standard criterion to diagnose pancreatic pseudocysts, other 
Imaging modalities like EUS can help in differentiating pseudocysts from other cystic 
lesions. (3) 
Pseudocyst fluid has high amylase levels and shows inflammatory cells on cytology. ERCP 
AND MRCP are other diagnostic modalities. 
Most pseudocysts resolve without interference, initial management of pseudocysts is 
conservative although some require drainage in case of symptomatic or complicated 
pseudocysts by the percutaneous catheter-based method. 
According to “ The rule of 6 of pancreatic pseudocysts “ a cyst >6cm/duration of > 6 weeks 
and a wall thickness of more than 6mm requires surgical intervention (4) Surgical drainage 
has been the traditional approach for pancreatic pseudocysts.  However, there is increasing 
evidence that transgastric and transduodenal endoscopic drainage are safe and effective 
approaches for patients with pancreatic pseudocysts in close contact  (defined as  <1  cm) 
with the stomach and duodenum,  respectively.  Also,  transpapillary drainage can be 
attempted in pancreatic pseudocysts communicating with the main pancreatic duct.  For 
patients in whom a  pancreatic duct stricture is associated with a  pancreatic 
pseudocyst,  endoscopic dilation and stent placement are indicated. Surgical drainage is 
indicated for patients with pancreatic pseudocysts that cannot be treated with endoscopic 
techniques and for patients who fail to respond to endoscopic treatment.  
Definitive treatment depends on the location of the cyst.  Pancreatic pseudocysts closely 
attached to the stomach should be treated with a  cystogastrostomy.  In this procedure,  an 
anterior gastrostomy is performed.  Once the pseudocyst is located,  it is drained through the 
posterior wall of the stomach using a  linear stapler. The defect in the anterior wall of the 
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Suresh and C P: A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis
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stomach is closed in two layers.  Pancreatic pseudocysts located in the head of the pancreas 
that is in close contact with the duodenum are treated with a 
cystoduodenostomy.  Finally,  some pseudocysts are not in contact with the stomach or 
duodenum.  The  surgical  treatment  for  these patients  is  a  Roux-en-
Y  cystojejunostomy(5) 
 
 
References 
1.Williams, Norman, P. Ronan O’Connell, and Andrew McCaskie. 2018. Bailey & Love’s 
Short Practice of Surgery, 27th Edition 
2. Habashi S, Draganov PV. Pancreatic pseudocyst. World J Gastroenterol. 2009;15(1):38-47. 
doi:10.3748/wjg.15.38 
3. Udeshika WA, Herath HM, Dassanayake SU, Pahalagamage SP, Kulatunga A. BMC 
Research Notes. 2018 Apr 27; 11: 262 
4. Wang GC, Misra S. A giant pancreatic pseudocyst treated by cystogastrostomy. BMJ Case 
Rep. 2015;2015:bcr2014207271. Published 2015 Mar 24. doi:10.1136/bcr-2014-207271 
5.Mattox. Sabiston Textbook of Surgery: The Biological Basis of 
Modern SurgicalPractic. 20th edition. Philadelphia, PA: Elsevier Saunders, 2017. 
 
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DOI: –


A Case Of Pancreatic Pseudocyst Following Acute Pancreatitis

Singhal, Medha

Prasad, Rajendra

Babu, Suresh

M, Manthappa

Digital Journal of Clinical Medicine 
Volume 2 Issue 1 Article 8 
1-1-2020 
Chronic Liver Disease 
Medha Singhal 
JSS AHER 
Rajendra Prasad 
JSS AHER 
Suresh Babu 
JSS AHER 
Manthappa M 
JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/djcm 
 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
and Pharmaceutical Sciences Commons, and the Public Health Education and Promotion Commons 
Recommended Citation 
Singhal, Medha; Prasad, Rajendra; Babu, Suresh; and M, Manthappa (2020) "Chronic Liver Disease," Digital 
Journal of Clinical Medicine: Vol. 2: Iss. 1, Article 8. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Chronic Liver Disease 
Medha Singhal, Dr.S.Rajendra Prasad, Dr.Suresh Babu, Dr.Manthappa, Dr.Varsha T, 
Department Of General Medicine, JSS Medical College, JSS AHER, Mysuru 
CLINICAL HISTORY: 
A 32 year old male patient presented with 
• Swelling of Bilateral lower limbs since 1 month. 
• Hypo pigmented skin lesions on nose, arms, chest since 3 months. 
• Distension of abdomen since 15 days 
• Yellowish discoloration of sclera since 4 days 
• Pain abdomen since 4 days 
• Breathlessness since 2 days 
 
PAST HISTORY 
No similar complaints in the past 
 
PERSONAL HISTORY 
Non smoker 
Alcoholic 270 ml/day since 8 years, last drink 1 week ago 
Sleep- disturbed 
Appetite-decreased 
EXAMINATION AND INVESTIGATIONS: 
GPE 
32 year old patient who is moderately built and nourished, well oriented 
pallor + 
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Icterus ++ 
B/L pedal edema + 
Hypopigmented skin on nose, chest, arms. 
 
 
 
 
No lymphadenopathy, clubbing , cyanosis, flapping tremors 
VITALS : 
PR:86bpm , regular 
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BP:130 /90 mm of Hg 
RR: 16 cycles/ min 
SpO2:99%at RA 
 
Hb :10.7 g/dl 
TLC:11070 cells/cumm 
ESR :85mm (raised) 
PCV : 29.8% 
RBC: 3.25mil/cumm 
Platelet:1.89 lakh /cumm 
Reticulocyte : 1.4% 
PBS: normocytic normocromic anemia 
with neutrophilic leukocytosis, rouleax formation, target cells present . 
RDW: 17.7 % 
Na : 128mEq/L 
Urine Routine : normal 
Anti-HIV , HBSAG , 
HCV : antibodies were nonreactive 
LFT : 
Total bilirubin:5.35mg/dL 
Direct bilirubin:3.61mg/dL 
Serum albumin :1.6g/dL 
AST:170 
ALT:25 
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PT,APTT,INR : Normal 
Ammonia :55micromoles/L(16 to 60) 
Serum Fe : 37.96µg/dL TIBC : 109µg/dL Serum ferritin:970.3ng/ml 
Chest X-Ray :B/L CP angle blunting 
USG abdomen: 
Cirrhosis of liver , 
Moderate ascites, 
Bilateral pleural effusions, Left > Right. 
Upper GI Endoscopy 
Palatal ulcer with early esophageal varices. 
Sub mucosal nodule with features of portal hypertensive gastropathy 
Skin biopsy was done which was suggestive of Discoid Lupus Erythematosis (DLE) 
 
FINAL DIAGNOSIS: 
Chronic liver disease with portal hypertension with signs of liver cell failure with Discoid 
Lupus Erythematosus 
 
Treatment Given: 
Inj Furosemide 40 mg Stat IV. Later 20 MG 1-1-0 
Tab Ursodeoxycholic acid 300 mg 1-0-1 
Inj Thiamine in 100  ml NS 0-1-0 
Inj Ceftriaxone 1gm IV 1-0-1 
Tab Propranolol  40 mg 1-0-0 
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Tab Spironolactone 25 mg 1-0-0 
Topical Steroids and Sun screener was advised by the dermatologist Patient was asked to 
come for follow up for further evaluation. But was lost for follow up. 
DISCUSSION: 
The three most widely recognised forms of Alcoholic Liver Disease are alcoholic fatty liver 
(steatosis), acute alcoholic hepatitis, and alcoholic cirrhosis. At least 80% of heavy drinkers 
develop steatosis, 10%–35% develop alcoholic hepatitis, and approximately 10% will 
develop cirrhosis [1] 
There is a clear dose-dependent relation between alcohol intake and the incidence of 
alcoholic cirrhosis. A daily intake of more than 60 g of alcohol in men and 20 g of alcohol in 
women significantly increases the risk of cirrhosis. In addition, daily drinking, as compared 
with binge drinking, appears to be more harmful.[2] 
Symptoms may not be visible in early stages 
1) Pain and swelling in abdomen 
2) Decreased appetite and weight loss 
3) Nausea and vomiting 
4) Fatigue 
 
Severe and specific symptoms can include encephalopathy and hepatic fever. [3] 
Clinical presentation is similar to other forms of end-stage liver disease but may be 
accompanied by concurrent alcoholic hepatitis. Spider angiomata, along with palmar 
erythema, enlargement of parotid and lacrimal glands, testicular atrophy, ascites, venous 
collaterals, jaundice and encephalopathy.[3] 
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Alcoholic fatty liver disease: Steatosis is invariable if consumption exceeds 80 g of alcohol 
per day. It is reversible with abstinence but may progress to cirrhosis if excess alcohol intake 
persists.[4] 
In this case during the analysis of LFT, AST is more than ALT, which is characteristic 
feature of Alcoholic liver disease[5] 
Discoid lupus erythematosus (DLE) is a chronic and common form of cutaneous lupus — a 
form of skin inflammation of unknown cause. It occurs particularly on sun-exposed skin, 
such as the face, ears, and scalp, but occasionally is much more extensive, involving large 
areas of skin. Permanent scarring can occur if treatment is delayed. [6] 
Local steroids, with sun screeners are tried. For severe cases anti-inflammatory drugs like 
Hydroxy chloroquine and immunosuppressant are tried.[6,7] 
REFERENCES:  
 
1. Grant BF, Dufour MC, Harford TC (1988) Epidemiology of alcoholic liver disease. 
Semin Liv Dis 8:12–25 
2. Grant BF, Dufour MC, Harford TC. Epidemiology of alcoholic liver disease. Semin 
Liver Dis 1988; 8(1):12–2 
3. Maddrey WC. Alcoholic hepatitis: clinicopathologic features and therapy. Semin 
Liver Dis 1988; 8(1):91–102. 
4. Teli MR, Day CP, Burt AD, et al.(1995) Determinants of progression to cirrhosis or 
fibrosis in pure alcoholic fatty liver. Lancet 346:987–990. 
5. Marsano, L.S.; Mendez, C.; Hill, D.; et al. Diagnosis and treatment of alcoholic liver 
disease and its complications. Alcohol Research & Health 27(3):247–256, 2003. 
6. Jessop S, Whitelaw DA, Grainge MJ, Jayasekera P. Drugs for discoid lupus 
erythematosus. Cochrane Database of Systematic Reviews. 2017(5). 
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7. Moura Filho JP, Peixoto RL, Martins LG, Melo SD, Carvalho LL, Pereira AK, Freire 
EA. Lupus erythematosus: considerations about clinical, cutaneous and therapeutic 
aspects. Anais brasileiros de dermatologia. 2014 Feb;89(1):118-25. 
 
 
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