Research Connect

N R, Dr. Rakshith

Reddy, Dr. Pranahith V

M, Dr. Kishor

Digital Journal of Clinical Medicine 
Volume 3 Issue 2 Article 9 
1-1-2021 
A Case of Moderate Clinical Depression in Early Onset Parkinson’s 
Disease 
Dr. Rakshith N R 
JSS AHER 
Dr. Pranahith V. Reddy 
JSS AHER 
Dr. Kishor M 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
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Recommended Citation 
N R, Dr. Rakshith; Reddy, Dr. Pranahith V.; and M, Dr. Kishor (2021) "A Case of Moderate Clinical 
Depression in Early Onset Parkinson’s Disease," Digital Journal of Clinical Medicine: Vol. 3: 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 Moderate Clinical Depression in Early Onset Parkinson’s Disease 
 
 Dr. Rakshith N R INTERN JSSMC, Dr. Pranahith V Reddy POST GRADUATE IN 
DEPARTMENT OF PSYCHIATRY Dr. Kishor M ASSOCIATE PROFESSOR OF 
PSYCHIATRY, JSS HOSPITAL 
 
CLINICAL HISTORY 
A 35-year-old female, married and having two children, studied till 7th Std, a 
homemaker from a lower-middle socio-economic section, Referred from Department of 
Neurology to Department of  Psychiatry, JSS Hospital with complaints of low backache, 
neck pain, sadness in the past 3-4 weeks, more so in last 15 days. She was normal 15 
days back, when she developed pain in the neck, dragging sensation in lower limbs, 
unable to do household chores.   She reported sadness for the past 15 days, decreased 
interaction with family, crying spells, disturbed sleep, and decreased interest in 
activities along with death wishes occasionally on and off. 
 
PAST HISTORY 
The patient had been diagnosed with Parkinson’s Disease at age 32 years and was on 
regular medication. She also had migraines and was taking medications only during 
migraine episodes. No h/o trauma, syncope, falls weakness, and paralysis. No menstrual 
abnormalities, no history of hypertension, diabetes mellitus, thyroid disorder. No 
significant psychiatric history in the family.  
 
 
EXAMINATION AND INVESTIGATIONS 
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N R et al.: A Case of Moderate Clinical Depression in Early Onset Parkinson’s
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VITALS: PR-80bpm BP-130/80mm of Hg RR-15cpm General physical examination: No 
pallor, Icterus, cyanosis, clubbing, edema, and lymphadenopathy. Mood – Subjectively 
she felt low. 
 
Objective– Depressed General appearance and behavior- well kept and groomed. 
Speech- normal Memory- normal Mood- depressed Mild  Resting Tremors were noticed 
in both hands The face was with less expression. Small stepping gait 
 
CNS: Higher mental functions- Intact Cranial nerves- Intact Sensory system- Normal 
Motor system- Normal Cerebellar functions- normal Reflexes- normal No paucity in 
range of motion, No rigidity. CVS- S1S2+, No murmurs 
 
RS– B/l Air entry + , B/l NVBS+ , No added sounds Per Abdomen: Soft, Non-tender, No 
organomegaly 
 
CT BRAIN– PLAIN  NORMAL STUDY 
THYROID PROFILE 
TSH-4.8 
 T3 – 110ng/dl 
 T4- 9 mcg/dl 
Fasting Blood Sugar-90 mg/dl 
Post-Prandial Blood Sugar – 130mg/dl 
HbA1c- 5.8 
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Complete Blood Count  – Normal blood picture 
PATIENT ASSESSMENT: 
Patient health questionnaire (PHQ-9) – 07/27 
HAMILTON DEPRESSION RATING SCALE (HAM-D) 
SCORE- 09 
DIAGNOSIS 
The patient was diagnosed with Moderate Depression (as per WHO ICD-10 Criteria) 
with Parkinson’s Disease 
 
DISCUSSION 
Parkinson’s Disease and Psychiatry conditions are closely associated. Parkinson’s disease 
(PD) is the second most common neurodegenerative disease worldwide, affecting 1-2% of 
the population with the usual age of onset being above 65 years[1].  These patients mainly 
present with motor symptoms like bradykinesia, resting tremors, and rigidity. However, 5-
10% of these cases present with symptoms at an early age (below 40 years) and is known as 
EARLY ONSET PARKINSON DISEASE(EOPD). Mutation in the Parkin gene is reported to 
be a major cause of EOPD with an autosomal recessive inheritance pattern[2]. 
The etiology of depression in PD is complicated and may result from changed serotonin (5-
HT) brain chemistry that is separate from the central dopaminergic deficiency associated with 
PD motor symptoms. Damage to Dopaminergic, serotonergic, noradrenergic, and cholinergic 
systems contribute to cognitive and behavioral dysfunctions in these patients[3]. 
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N R et al.: A Case of Moderate Clinical Depression in Early Onset Parkinson’s
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The incidence of depression in EOPD is greater than that in the late-onset variant. EOPD 
significantly reduces the patients’ quality of life and it’s also one of the conditions which go 
undiagnosed or undertreated. 
The interaction between depression and PD is bidirectional i.e PD increases the risk for 
depression and vice versa[4]. 
 When treating a patient with both PD and Depression, it’s observed that depressed patients 
take a significantly higher dose of levodopa for a longer duration, and also have a 
significantly higher depression score. Treating the patients with levodopa indirectly interferes 
with serotonergic function in the CNS by its competition for uptake, storage, and metabolism 
of serotonin. Treatment with antidepressants reverses the effect of levodopa on serotonin (5-
hydroxytryptamine; 5-HT). Some patients report exacerbated depressive episodes on taking 
levodopa , in conditions where antiparkinsonian efficacy is less. A few patients with previous 
history of depressive episodes have reported attempting suicide after taking Levodopa[5][6]. 
Patients with early-onset PD are particularly vulnerable to depression as a reaction to the 
illness’s detrimental effect on their careers, financial security, and quality of life during their 
most productive years. The early onset of PD causes ‘premature social aging’, whereby the 
level of social handicap is inconsistent with the patient’s age and may further contribute to 
the risk factors for depression[7]. 
Antidepressants like Amitriptyline(TCA), SSRI can be used to treat the depressive symptoms 
associated with PD[2]. 
MESSAGE:  Early identification of Depression in the Non-motor symptom complex of 
Parkinson’s disease, especially in EOPD, and appropriate diagnosis and treatment of the 
associated condition would go a long way in reducing the social, mental, physical, and 
economic burden on the patient[4]. 
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ACKNOWLEDGEMENTS: None  
 
REFERENCES 
 
1) Grover S, Somaiya M, Kumar S, Avasthi A. Psychiatric aspects of Parkinson’s 
disease. Journal of neurosciences in rural practice. 2015 Jan;6(1):65.   
2) Rizek P, Kumar N, Jog MS. An update on the diagnosis and treatment of Parkinson 
disease. Cmaj. 2016 Nov 1;188(16):1157-65.   
3)Grosch J, Winkler J, Kohl Z. Early degeneration of both dopaminergic and 
serotonergic axons–a common mechanism in Parkinson’s disease. Frontiers in cellular 
neuroscience. 2016 Dec 22;10:293. 
4) ESER HY, BORA HA, KURUOĞLU A. Depression and Parkinson disease: 
prevalence, temporal relationship, and determinants. Turkish Journal of Medical 
Sciences. 2017 Apr 18;47(2):499-503. 
5) Tom T, Cummings JL. Depression in Parkinson’s disease. Drugs & aging. 1998 
Jan 1;12(1):55-74. 
6) Frisina PG, Haroutunian V, Libow LS. The neuropathological basis for depression 
in Parkinson’s disease. Parkinsonism & related disorders. 2009 Feb 1;15(2):144-8. 
7) Schrag A. Quality of life and depression in Parkinson’s disease. Journal of the 
neurological sciences. 2006 Oct 25;248(1-2):151-7. 
8)Tandberg E, Larsen JP, Aarsland D, Laake K, Cummings JL. Risk factors for 
depression in Parkinson disease. Archives of Neurology. 1997 May 1;54(5):625-30. 
 
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N R et al.: A Case of Moderate Clinical Depression in Early Onset Parkinson’s
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English

A Case of Moderate Clinical Depression in Early Onset Parkinson’s Disease

Tripathi, Nikita

Thammaiah, Dr Adarsh

Digital Journal of Clinical Medicine 
Volume 3 Issue 3 Article 8 
1-1-2021 
A Case of Atypical Presentation of Radial Nerve Injury 
Nikita Tripathi 
JSS AHER 
Dr Adarsh Thammaiah 
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 
Tripathi, Nikita and Thammaiah, Dr Adarsh (2021) "A Case of Atypical Presentation of Radial Nerve Injury," 
Digital Journal of Clinical Medicine: Vol. 3: Iss. 3, 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. 
A Case of Atypical Presentation of Radial Nerve Injury 
 
Nikita Tripathi [7th Term MBBS], Dr Adarsh Thammaiah, Department Of Orthopaedics, JSS 
Medical College, JSSAHER, Mysuru  
 
CASE REPORT: 
CLINICAL HISTORY: 
 
A 12 year old male patient was admitted at JSS Hospital with complaints of inability to 
extend his right wrist and fingers . The patient gives a history of self fall from a cycle 1 week 
back , following which he complained of severe pain and deformity of his right arm. Pain was 
sudden in onset and aggravated on movement of the arm and relieved on immobilisation. 
There was severe tenderness in the lower arm. Deformity and crepitus was felt on movement. 
Patients could perform active movements of the elbow, wrist and fingers. 
X ray of the right arm was taken and was diagnosed with fracture of the right humerus. 
Fracture was transverse type at the junction of the middle and lower 1/3rd shaft which was 
displaced.  
Closed reduction was done and the above elbow POP slab was applied and planned to treat it 
conservatively. No neurovascular deficit was seen. 
Later after 4-5 days, the patient reviewed back to opd with complaints of not being able 
to  extend his wrist and fingers with loss of sensation over the 1st web space.  
Slab was removed and examination of the right upper limb was done. 
 
EXAMINATION AND INVESTIGATIONS: 
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Tripathi and Thammaiah: A Case of Atypical Presentation of Radial Nerve Injury
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Attitude 
The arm was rested on the bed with 90 degrees flexion at the elbow. There appeared to be a 
wrist drop deformity with complete flexion at the wrist and mild flexion at the MCP and IP 
joints. 
Inspection  
Skin over the arm appeared to be normal 
There was mild diffuse swelling over the middle and distal part of the arm. 
Palpation  
No local rise in temperature 
Sensation over the 1st web space on the dorsal side of the hand was reduced. 
Motor power of  
Triceps 5/5 
ECRL and ECRB 0/5 
Brachioradialis 0/5 
Extensor digitorum 0/5 
Extensor carpi ulnaris0/5 
Extensor indices0/5 
Extensor digiti minimi0/5 
Distal pulses palpable 
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PRE-OP X-ray 
 
 
AP and Lateral X-ray of right humerus showing transverse fracture of mid and lower 1/3rd of 
right humerus along with displacement.   
 
 
Picture showing wrist drop 
 
 
FINAL DIAGNOSIS: 
 
Fracture of the shaft of humerus with wrist drop secondary to lower radial nerve injury 
probably due to neuropraxia. 
 
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Tripathi and Thammaiah: A Case of Atypical Presentation of Radial Nerve Injury
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DISCUSSION:  
 
TREATMENT:  
Exploration of the radial nerve was done. There was no nerve entrapment or contusion 
seen.  Open reduction of the fracture and fixation with plate and screws was done. 
Dynamic cockup splint was applied to the wrist and fingers to maintain the length and tone of 
the muscle and prevent any muscular contraction. 
 
 
 
Picture showing fracture reduction with plate and screws and radial nerve crossing over the 
lower part of the plate from medial to lateral 
 
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POST OP Xray showing humerus fracture reduced and fixed with plate and screws  
 
 
Picture showing dynamic cockup splint 
 
RADIAL NERVE INJURY  
Root Value: C5-T1; Branch of posterior cord of brachial plexus  
RADIAL NERVE IN THE ARM 
1. Muscular branches 
▪ long and medial head of triceps [before entering spiral groove] 
▪ lateral and medial head of triceps [in the spiral groove] 
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Tripathi and Thammaiah: A Case of Atypical Presentation of Radial Nerve Injury
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▪ brachialis , brachioradialis , ECRL [below the spiral groove] 
2. Cutaneous  branches 
▪ posterior cutaneous nerve of the arm [above the radial groove] 
▪ lower lateral cutaneous nerve of the forearm [in the radial nerve] 
RADIAL NERVE IN THE FOREARM  
▪ branches into superficial and deep terminal branches in the cubital fossa 
▪ superficial branch is cutaneous and distributed to the lateral half of the dorsum of the 
hand and to the proximal parts of the dorsal surface of the thumb, index, middle and 
lateral half of the ring finger 
▪ deep posterior interosseous branch supplies ECRB and part of supinator and after 
leaving supinator tunnel supplies EDC, EDM, EI, ECU, abductor pollicis  longus, 
extensor pollicis longus and brevis. [1] 
MODES OF INJURY 
1. In the axilla  
▪ aneurysm of the axillary vessels 
▪ crutch palsy 
2. In the shoulder 
▪ proximal humeral fractures 
▪ shoulder dislocation 
3. In the spiral groove 
▪ shaft fracture 
▪ saturday night palsy  
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▪ syringe palsy 
▪ surgical positions ( Tredelenburg) 
4. Between spiral groove and lateral epicondyle 
▪ fracture shaft humerus 
▪ supracondylar fracture humerus 
▪ lateral epicondyle fracture of the humerus 
▪ penetrating and gunshot injuries 
▪  cubitus valgus deformity  
5. At the elbow 
▪ posterior dislocation of the elbow 
▪ fracture head of humerus 
▪ Monteggia fractures. [2] 
LEVEL OF LESION 
1. High (above spiral groove) 
▪ total palsy 
1. Low type I (between the spiral groove and the lateral epicondyle) 
▪ wrist drop 
▪ thumb drop 
▪ finger drop 
▪ loss of sensation in dorsum of first web space 
1. Low type II (below the elbow) 
▪ thumb drop 
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Tripathi and Thammaiah: A Case of Atypical Presentation of Radial Nerve Injury
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▪ finger drop 
▪ loss of sensation over the first web space. [2] 
EXAMINATION 
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HOLSTEIN LEWIS FRACTURE-  It is a long spiral fracture of the lower one third of 
humerus leading to entrapment of radial nerve  
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Tripathi and Thammaiah: A Case of Atypical Presentation of Radial Nerve Injury
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 But in this case,                                                                                                                         
1. Patient presented with Radial nerve injury after 5 days of application of the U slab  
2. Fracture is lower to the radial groove 
3. Fracture is transverse type  and not the spiral    
4. Intraoperatively no entrapment of the radial nerve was observed.  
So this was an unusual presentation of radial nerve injury with fracture of the humerus, where 
the cause is still unknown. 
 
CONCLUSION: 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
 
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Digital Journal of Clinical Medicine, Vol. 3 [2021], Iss. 3, Art. 8
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DOI: –
1. Chaurasia BD. Human Anatomy: regional and applied dissection and clinical. 7th ed. 
Vol. 1. New Delhi: CBS Publishers & distributors Pvt Ltd; 2016. 
2. Ebnezar J. Textbook Of Orthopedics (Includes Clinical Examination Methods In 
Orthopaedics). 5th ed. Vol. 1. New Delhi: Jaypee Brothers Medical Publishers (P) 
Ltd.; 2017. 
3. Blom Ashley, Warwick D, Whitehouse M, editors. Apley & Solomon’s System of 
Orthopaedics and Trauma. 10th ed. United Kingdom: CRC Press; 2017. 
4. https://en.wikipedia.org/wiki/Holstein-Lewis_fracture  
 
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A Case of Atypical Presentation of Radial Nerve Injury

Anusha, Dr.Pogula

Reddy, Dr.Pranahit

Digital Journal of Clinical Medicine 
Volume 3 Issue 1 Article 8 
1-1-2021 
A Case of Premature Ejaculation 
Dr.Pogula Anusha 
JSS AHER 
Dr.Pranahit Reddy 
JSS AHER 
Dr. Kishor 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 
Anusha, Dr.Pogula; Reddy, Dr.Pranahit; and M, Dr. Kishor (2021) "A Case of Premature Ejaculation," Digital 
Journal of Clinical Medicine: Vol. 3: 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. 
A Case of Premature Ejaculation 
Dr.Pogula Anusha,  
Dr.Pranahit Reddy,  
Dr.Kishore.M  
 
CLINICAL HISTORY: 
Mr. N,36 years male studied till 10th class, a farmer by occupation from a rural background, 
married 5 months ago, presented to the Psychiatry outpatient department with a complaint of 
difficulty during sexual intercourse. From the time of marriage, the patient reported that they 
had difficulty to consummate the marriage. The patient was worried about the sexual acts and 
he would ejaculate before initiating penetrative sex. 
These thoughts made him anxious while carrying out sexual activity. The couple had a 
cordial relationship between them. The patient had the normal desire and arousal was not a 
problem but had difficulty initiating penetrative sex. The patient was preoccupied with 
thoughts of failed penetrative sex and concerns about the possibility of not having children. 
The patient’s wife, aged 18years, corroborated the given history. The patient had no history 
of substance abuse, persistent sadness, hypertension, diabetes mellitus, thyroid problem. 
The patient had a past history of episodes of anxiety with autonomic symptoms and had taken 
treatment 3 years ago for a period of 3 months. Details were not available. No family history 
of psychiatric illness 
 
EXAMINATION AND INVESTIGATIONS: 
General physical examination: 
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Moderately built and nourished. 
 The patient is conscious, coherent, cooperative. 
General physical and systemic examination was within normal limits. 
Genital examination: no abnormality observed. 
Mental Status Examination: The patient was well-groomed, cooperative, and oriented to time, 
place, and person. 
Thoughts: preoccupied with thoughts regarding his sexual dysfunction. 
The mood was Anxious, with insight 3/6 
ASSESSMENT: 
ASEX (Arizona Sexual Experiences Scale score):16 
Possible total scores range between 5 and 30, higher scores indicating greater sexual 
dysfunction. 
 
FINAL DIAGNOSIS: 
Premature ejaculation. 
ICD-10 diagnostic guidelines: The inability to control ejaculation sufficiently for both 
partners to enjoy sexual interaction. In severe cases, ejaculation can occur before vaginal 
entry or in the absence of an erection. 
 
DISCUSSION:  
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People in India, more from rural backgrounds have many myths and misconceptions about 
sexual intercourse, and sex education is considered a topic of taboo that leads to a lack of 
sexual knowledge. However, there is assumed sociocultural pressure over conceiving 
immediately after a marriage that adds up to anxiety. This case highlights the need for sex 
education in schools and communities [1]. 
Also, premarital counseling would help in these scenarios. Premature ejaculation is one of the 
most common sexual dysfunctions reported which is wrongly assumed as erectile 
dysfunction. A detailed history helps in clarification[2]. 
 Nonpharmacological methods such as the “Start and stop” technique and the Penile 
“Squeeze” technique are known to beneficial and delayed ejaculation, which is a known 
adverse effect of SSRI medications is utilized in the treatment of premature ejaculation in 
many patients with satisfactory outcomes [3]. 
Premature ejaculation is one of the most common male sexual disorders and has been 
estimated to occur in 4-39% of men in the general community [4]. 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
 
1. Ismail S, Shajahan A, Sathyanarayana Rao TS, Wylie K. Adolescent sex education in 
India: Current perspectives. Indian J Psychiatry. 2015;57(4):333-337. doi:10.4103/0019-
5545.171843 
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2. Rajkumar RP, Kumaran AK. The association of anxiety with the subtypes of premature 
ejaculation: a chart review. Prim Care Companion CNS Disorders. 2014. Published 2014 Jul 
31. 
3. Avasthi A, Grover S, Sathyanarayana Rao TS. Clinical Practice Guidelines for 
Management of Sexual Dysfunction. Indian J Psychiatry. 2017;59(Suppl 1):S91-S115. 
doi:10.4103/0019-5545.196977 
4.  McMahon C. Premature ejaculation. Indian Journal of Urology. 2007;23(2):97. 
 
 
 
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A Case of Premature Ejaculation

Nallathambi, Nikita

BS, Dr. Rakesh

Digital Journal of Clinical Medicine 
Volume 3 Issue 3 Article 10 
1-1-2021 
URTI Associated with Reuse of Mask during COVID 19 
Nikita Nallathambi 
JSS AHER 
Dr. Rakesh BS 
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 
Nallathambi, Nikita and BS, Dr. Rakesh (2021) "URTI Associated with Reuse of Mask during COVID 19," 
Digital Journal of Clinical Medicine: Vol. 3: 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. 
URTI Associated with Reuse of Mask during COVID 19 
 
R. Nikita Nallathambi; Dr. Rakesh BS , Department Of ENT, JSS Medical College, 
JSSAHER, Mysuru 
 
CLINICAL HISTORY: 
39 year old doctor presents to ENT OPD with history of throat irritation for the last 2 weeks. 
He felt the constant urge to take menthol based lozenges. He had no history of cough or 
fever. The doctor would use N95 mask, most of the days but had limited supply of N95 
masks, hence frequently reuse them after UV sanitization.  
There is no history of comorbidities.  
No habits. 
EXAMINATION AND INVESTIGATIONS: 
General physical examination- a middle aged male , moderately built and nourished, alert 
conscious and cooperative and  well oriented to time, place and person. 
Pulse: 86 bpm 
BP: 130/80 mmHg 
Respiratory rate: 18 cpm 
Temperature: 98.2 F 
No pallor,icterus, cyanosis, clubbing, edema, lymphadenopathy 
ENT examination  
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Ear and nose examination: NAD 
Throat examination revealed mild congestion of posterior pharyngeal wall with no other 
abnormality. 
SYSTEMIC EXAMINATION: 
RS: b/l NVBS, No added sounds 
CVS: S1,S2 heard, no murmurs 
P/A: Soft, non-tender.  
CNS: No focal neurological deficits 
AEC: 500 
COVID RT-PCR: Negative 
FINAL DIAGNOSIS: 
Rhinopharyngitis 
DISCUSSION:  
Tab. AZITHROMYCIN 500mg 0D x 3 days 
Tab. FEXOFENADINE 120mg OD x 7 days (because patient had h/o drowsiness with 
Cetrizine/ levocetrizine) 
Patient was advised salted warm water gargling as needed. 
Patient was also advised to reduce the reuse of N95 masks. 
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COVID19 Pandemic is unprecedent in recent time and wearing mask is now considered 
norm, and lifesaving. More so in health workers, masks are worn for most of the time in a 
day. In recent time, the emergence of life-threatening infections such as severe acute 
respiratory syndrome (SARS) and re-emerging infectious diseases like tuberculosis have 
highlighted the need for efficient infection control in all health care settings. Health care 
workers (HCW) who are routinely exposed to viral respiratory infections in the workplace 
may get infected and transmit infection to others.(1) Following of the infection control 
guidelines including that for COVID19, hand hygiene and masks cause a breach in spread of 
infection and therefore ensure safety to HCW, patients and close contacts.  
A surgical mask protects HCW from inhaling pathogens transmitted by the droplet route such 
as varicella and meningococcal diseases. Medical masks prevent hand-to-face contact and 
facial contact with large droplets and sprays while protecting the mucous membranes of nose 
and mouth. An N95 mask protects HCW from respiratory pathogens transmitted as aerosols 
which may even be less than 5 microns and can remain suspended in the air for a long period 
of time especially when bounded by dust. This helps to prevent the spread of infectious 
diseases such as TB, MDR-TB, pulmonary plaque, measles,etc..(1) Elastomeric full-face 
N95s, N100s, and self-contained breathing apparatuses provide full protection but are their 
availability is limited and hence reserved for critical procedures with high contamination risk. 
These devices should be cleaned and decontaminated as per standard procedures, which may 
be labor-intensive.(2)  
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N95 indicates that they are not resistant to oil or solvents (N) and that they are intended to 
filtrate at least 95% of airborne particles >0.3 µm in size. N95 filters are made of several 
layers of woven synthetic material treated to sustain an electrostatic charge (i.e., an electret). 
In addition to creating a mechanical barrier against aerosols, N95 filters retain charged 
particles, such as bacteria. However, N95 filters provide no protection against fumes, oils, or 
vapors(2) 
A study conducted by Peng Yangl et al on mask wearing and respiratory infection in HCW in 
Beijing in showed that out of 400 subjects 336 developed adverse effects which included 
allergy, breathing difficulty, discomfort, pain. 59.5% developed (RTI ) respiratory tract 
infection  (defined as having at least 2 of the following symptoms fever, cough, sore throat, 
nasal congestion, rhinorrhea). The study also proved that the cloth/cotton yarn masks that are 
widely used are less efficacious than medical masks.(3) 
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Single-use N95 respirators are important to protect staff and patients from airborne 
infections, but shortages may occur during disease outbreak or any similar crisis which can 
be prevented by extended wear(wearing N95 for hours at a time)or reusing it several times. 
(2) 
Reusing masks without cleaning can cause bacteria, virus, dust and allergens to accumulate 
which can pass on to the throat causing irritation and strain. Individuals with weaker 
immunity and those with history of allergy are more prone to it.  
URTI due to reuse of mask is a frequent complaint especially among health care works as 
there is a need for them to wear masks for prolonged time periods. Shortage of respirators 
have led to reuse of respirators. (4) 
Comprehensive guidelines released by the All India Institute of medical sciences (AIIMS), 
New Delhi on Standard operating procedures for extended use of N-95 masks for HCW 
advises to use 4 masks with fifth mask kept as reserve. The masks are used in order up to 5 
times and are to be discarded in the yellow bin after 20 days of use. These masks cannot be 
treated and reused as the filtering capacity of mask reduces.(5) 
To prevent sore throats due to masks, all health care workers should be educated and advised 
to change masks regularly and avoid touching masks in frequent intervals. 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
1. World Health Organization, Regional Office for the Western Pacific, World Health 
Organization, Regional Office for South-East Asia. Practical guidelines for infection control 
5
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in health care facilities. Manila; New Delhi: World Health Organization, Regional Office for 
Western Pacific ; World Health Organization, Regional Office for South-East Asia; 2004. 9 
p.  
2. Emergency Care Research Institute. 8697 – Safety of Extended Use and Reuse of N95 
Respirators. 2020 Mar;1–6.  
3. Mask-wearing and respiratory infection in healthcare workers in Beijing, China [Internet]. 
[cited 2020 Nov 29]. Available from: 
https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702011000200002 
4. Why are some people getting a sore throat from wearing a mask? – Times of India 
[Internet]. [cited 2020 Nov 29]. Available from: https://timesofindia.indiatimes.com/life-
style/health-fitness/health-news/why-are-some-people-getting-a-sore-throat-from-wearing-a-
mask/articleshow/78320898.cms 
5. SOPs for extended use of N95 mask for personal safety of Health Care Workers (HCW) at 
AIIMS | AIIMS Covid Information Portal [Internet]. [cited 2020 Nov 29]. Available from: 
https://covid.aiims.edu/standard-operating-procedure-sop-for-extended-use-of-n95-mask-for-
personal-safety-of-health-care-workers-hcw-at-aiims/ 
 
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URTI Associated with Reuse of Mask during COVID 19

oai:rescon.jssuni.edu.in:radiologyteachingfiles-1004CLINICAL HISTORY: 
A 35-year-old male patient presented with history of massive hemoptysis associated with pain abdomen and breathlessness since the past 3 days. Patient had no prior co-morbidities; however was a chronic alcoholic and smoker since the past 15 years. No hospital admissions in the pas

Raj, Vinay, Dr

Kini, Divya Vishwanatha, Dr

Splenic artery pseudo-aneurysm secondary to necrotizing pancreatitis – A rare lethal complication.

CLINICAL HISTORY
70 year old male patient came with the complaints of weakness in bilateral lower limbs since 2 months and acute retention of urine since 20 days. Blood work-up was done and the parameters were within normal limits

Bawgi, Srikanth, Dr

Sheshadri, Roopa, Dr

C, Anupama, Dr

JSS Academy of Higher Education and Research 
Research Connect 
Radiology Teaching Files 
2021 
Spinal Schwannoma 
Srikanth Bawgi Dr 
Jss medical college 
Roopa Sheshadri Dr 
Jss medical college 
Anupama C Dr 
Jss medical college 
Follow this and additional works at: https://rescon.jssuni.edu.in/radiologyteachingfiles 
 Part of the Medicine and Health Sciences Commons 
Recommended Citation 
Bawgi, Srikanth Dr; Sheshadri, Roopa Dr; and C, Anupama Dr, "Spinal Schwannoma" (2021). Radiology 
Teaching Files. 3. 
https://rescon.jssuni.edu.in/radiologyteachingfiles/3 
This Neuroradiology is brought to you for free and open access by Research Connect. It has been accepted for 
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A. CASE TITLE: SPINAL SCHWANNOMA 
B. CLINICAL HISTORY – 70year old male patient came with the complaints of weakness in 
bilateral lower limbs since 2 months and acute retention of urine since 20days. Blood 
work-up was done and the parameters were within normal limits.  
        
C.IMAGING DIAGNOSIS: 
 
Figure 1     
X-ray CHEST – Ill defined homgenous opacity projected over the left hila, mid zone without 
silhouetting the left cardiac border – Likely posterior medistinal mass. 
 
Figures 2 : X-ray DORSOLUMBAR SPINE LATERAL         1
Bawgi et al.: Spinal Schwannoma
Published by Research Connect, 2021
 
 
X-ray DORSO LUMBAR SPINE (LATERAL)- Ill defined homgenous opacity with smooth margins 
occupying the middle and posterior medastinum – Likely posterior medistinal mass. 
Figures 3: MRI Thoracic-SPINE  
a) T1 sagittal    
 
b) T1 axial  
Fig: 3 a,b: Large dumb-bell shaped intradural extra-medullary mass arising from the spinal canal 
at the level of D8 vertebral body casuing the widening of left neural foramina. The lesion has 
small intradural component with a large extra spinal component in the left paravertebral region 
occupying majority of the left hemi-thorax. The lesion appears iso-hypointense on T1WI (Fig 
3a,b)   
 
 2
Radiology Teaching Files, Art. 3 [2021]
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c) T2 sagittal         
  
 
d) T2 axial      
Fig 3c,d : Heterogenously hyperintense on T2WI. 
 
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Bawgi et al.: Spinal Schwannoma
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Figure 4 :  MRI T1 post contrast sagittal.   
Fig 4: On post contrast images, the lesion shows heterogenous enhancement with central 
enhancing areas -Likely necrosis  
FINAL DIAGNOSIS : Large dumbell shaped intradural extra-medullary mass arising from the 
spinal canal at the level of D8 vertebral body – Likely nerve sheath tumour (Schwannoma). 
Histopathological diagnosis: Schwannoma. 
A. DISCUSSION 
Spinal schwannoma are benign nerve sheath tumors within the spinal canal, typically arising 
from the spinal roots and it is the second most common nerve sheath tumor of spine.   
Epidemiology 
Annual incidence is 0.4 /100,000. Comprise about 40-45% of all spinal tumors. The mean age is 
46 years with no sex predilection. 
Etiopathogenesis: Schwannomas originate from Schwann cells, derived from precursor cells in 
the embryonic neural crest. Majority are solitary and sporadic. However, there is association 
with Neurofibromatosis type2 (NF2). Loss of NF2 protein Merlin results in defective 
tumorogenesis in multiple tissues. NF2 tumor suppression gene located on chromosome 22, 
has high mutation rate and represent almost half of cases of NF2 with new mutations. 
General features: 
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Radiology Teaching Files, Art. 3 [2021]
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Most patients present with radicular pain / paresthesia, but can present with myelopathy 
including progressive paraparesis, if they occur in cervical or thoracic region. Weakness can 
occur later in the course of disease. 
B. IMAGING 
Primary diagnostic modality for EISTs is magnetic resonance imaging -MRI. Diagnostics also 
include plain X-ray imaging in antero-posterior, lateral and dynamic (flexion, extension) 
projections. Furthermore, Computerized tomography (CT) scan, thin cuts with reconstructions ( 
Bone window) are important to evaluate bony anatomy. In patients who could not undergo 
MRI scanning, CT myelography is an alternative.                    
 
CT findings: 
1. Schwannomas are slightly hypodense relative to paraspinal musculature. 
2. Giant schwannomas occurring within the lumbar spinal canal can cause marked bone 
remodeling of the spinal canal and neural foramina. 
3. Intradural schwannoma at myelography have characteristic “cap sign”, where contrast 
filled intrathecal CSF forms a meniscal cap above and/or below the intradural tumor. 
 
MRI findings:  
1. Modality of choice for diagnosing and assessing the extent of schwannomas. 
2. Foraminal schwannomas often have a intradural component giving them a dumbbell 
shaped configuration. 
3. These tumors are typically T1 hypointense or isointense relative to the spinal cord. 
4. And are T2 hyperintense to relative to spinal cord 
5. On contrast administration, solid portions usually enhance homogenously. Some 
enhance slightly more at the periphery. Cystic area commonly occurs within the an 
intradural schwannoma and does not enhance. 
 
 
Treatment: 
1. Conservative approach: Small intradural schwannomas found incidentally in the cauda 
equina are usually not treated until they become symptomatic. 
2. Surgical excision: In cases with significant neurologic dysfunction / uncontrollable pain 
or in case of malignant degeneration. 
    
 
REFERENCES – 
1. Arnautovic K, Arnautovic A. Extramedullary intradural spinal tumors: a review of modern 
diagnostic and treatment options and a report of a series. Bosnian journal of basic 
medical sciences. 2009 Oct;9(Suppl 1):S40. 
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2. Murphey MD, Smith WS, Smith SE, et al: From the archives of the AFIP. Imaging of 
musculoskeletal neurogenic tumors: Radiologic-pathologic correlation. Radiographics 
1999; 19: pp. 1253-1280 
3. Beaman FD, Kransdorf MJ, Menke DM. Schwannoma: radiologic-pathologic correlation. 
Radiographics. 2004 Sep;24(5):1477-81. 
4.  Beall DP, Googe DJ, Emery RL, et al: Extramedullary intradural spinal tumors: A pictorial 
review. Curr Probl Diagn Radiol 2007; 36: pp. 185-198 
5.  Kono K, Inoue Y, Nakamura H, et al: MR imaging of a case of a dumbbell-shaped spinal 
schwannoma with intramedullary and intradural-extramedullary components. 
Neuroradiology 2001; 43: pp. 864-867 
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Spinal Schwannoma

CLINICAL HISTORY
Presenting history – A 24 year old male patient came with complaints of haemoptysis since 3months, aggravated on exertion around 3-4 episodes per day with around 3-4 ml of frank blood. No complaint of chest pain/ fever. No past history of PTB. No e/o significant past history. Patient tested negative for HLA b51 and Anti-nuclear antibody

Kumar, Sanath, Dr

Das, Sudha Kiran, Dr

M, Gurumurthy, Dr

JSS Academy of Higher Education and Research 
Research Connect 
Radiology Teaching Files 
2021 
MULTIPLE PULMONARY ARTERY ANEURYSMS : A CASE REPORT 
OF PULMONARY VASCULITIS 
Sanath Kumar Dr 
JSS Medical College, JSS AHER 
Sudha Kiran Das Dr 
JSS Medical College, JSS AHER 
Gurumurthy M Dr 
JSS Medical College, JSS AHER 
Follow this and additional works at: https://rescon.jssuni.edu.in/radiologyteachingfiles 
Recommended Citation 
Kumar, Sanath Dr; Das, Sudha Kiran Dr; and M, Gurumurthy Dr, "MULTIPLE PULMONARY ARTERY 
ANEURYSMS : A CASE REPORT OF PULMONARY VASCULITIS" (2021). Radiology Teaching Files. 1. 
https://rescon.jssuni.edu.in/radiologyteachingfiles/1 
This Cardiovascular is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Radiology Teaching Files by an authorized administrator of Research Connect. 
MULTIPLE PULMONARY ARTERY ANEURYSMS : A CASE REPORT 
OF PULMONARY VASCULITIS 
CLINICAL HISTORY 
Presenting history – A 24 year old male patient  came with complaints of haemoptysis 
since 3months, aggravated on exertion around 3-4 episodes per day with around 3-4 ml 
of frank blood. No complaint of chest pain/ fever. No past history of PTB. No e/o 
significant past history. Patient tested negative for HLA b51 and Anti-nuclear antibody. 
Imaging  
  
 
Chest radiograph PA view Fig 1 - Few well-defined nodular opacities in bilateral peri-
hilar region and right lower zones. No e/o calcifications. Accentuated bronchovascular 
markings noted. 
 
              
                        Fig.2a                                                     Fig.2b 
Plain Computed tomography thorax Axial section - Fig 2a (lung window) and 2b 
(mediastinal window) - Multiple well-defined nodules in bilateral lung fields. No e/o 
calcifications/ air bronchogram. 
 
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Kumar et al.: MULTIPLE PULMONARY ARTERY ANEURYSMS : A CASE REPORT OF PULMONARY
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  Fig. 3 
CECT pulmonary angiogram Fig 3 - Axial section -  Multiple well-defined 
homogeneously enhancing nodules arising from segmental pulmonary artery with 
peripheral non enhancing areas – s/o Pulmonary aneurysms with thrombosis. 
 
    
                                          
                              4a                                                                   4b 
CECT pulmonary angiogram - Fig.4 a & 4b Coronal & sagittal section (mediastinal 
window)  
Well-defined homogeneously enhancing nodule arising from segmental branches of left 
lower pulmonary artery with peripheral non enhancing areas. Feeding artery sign noted 
in image 4b. 
 
 
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                          5a                                                           5b 
CECT pulmonary angiogram Fig.5 a & 5b Axial section (mediastinal window) - 
Near total resolution of the previously imaged pulmonary aneurysms post 
immunosuppressant’s therapy. 
 
 
 
 
CECT pulmonary angiogram Fig.6 Coronal section (mediastinal window) 
(mediastinal window) shows circumferential filling defect in postero-basal segment of left 
lower lobe artery – s/o chronic thrombosis. 
 
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Kumar et al.: MULTIPLE PULMONARY ARTERY ANEURYSMS : A CASE REPORT OF PULMONARY
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Fig.7 Chest radiograph PA view -Near total resolution of previously imaged nodules 
post immunosuppressant therapy. 
 
Follow up : There was near total resolution of the previously images nodules on 
follow up scans (Fig 5a, 5b, 6 & 7) post treatment with immunosuppressant’s (Pulse 
methyl-prednisolone & azathioprine).  
 
Differential diagnosis 
• Behcets disease. 
• Giant cell arteritis. 
• Takaysaus arteritis. 
 
Final diagnosis 
• Pulmonary vasculitis with multiple pulmonary aneurysms. 
 
Discussion  
Etiopathogenesis – 
Pulmonary artery aneurysms are rare & infrequently diagnosed. The causes can be 
congenital or acquired. 
Congenital - 
Persistent ductus arteriosus, atrial & ventricular septal defect, pulmonary valvular 
stenosis & regurgitation. Connective tissue disorders ( Ehler danlos & marfans 
syndrome). 
Acquired –  
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Vasculitis ( Behcets & giant cell arteritis), infections ( syphilis, tuberculosis & pyogenic 
bacteria), pulmonary arterial hypertension, neoplasms, & chronic pulmonary embolism. 
In ANCA-associated vasculitis, an intense infiltration of activated neutrophils results in 
fibrinoid necrosis and dissolution of vessel walls, thus compromising the vascular 
lumen5.  
Production of autoantibodies such as antiglomerular basement membrane antibody 
(type 2 hypersensitivity reaction), formation of immune complexes (type 3 
hypersensitivity reaction), and T cell involvement (type 4 hypersensitivity reaction) are 
likely to link to the pathogenesis of  small-vessel pulmonary vasculitis5.  
The damage to the integrity of the vessels results in the leakage of blood into the 
alveolar space from the interstitial capillaries and causes stenoses, thrombotic 
obstruction, and aneurysms of the corresponding vessels5.  
Most common and dreaded complication is haemoptysis.  
 
 
Imaging Features – 
Chest radiograph -  Dilatation of main pulmonary trunk, right & left main pulmonary 
artery. Interlobar arteries also shows increased size & opacity. Mediastinal widening due 
to thrombosis of the superior vena cava4. Well defined nodular opacities with peripheral 
calcifications can be seen in case of thrombosis of pulmonary artery aneurysms. 
 
CT findings –  
Aneurysmal dilation of segmental pulmonary arteries.  
Pulmonary aneurysms can be fusiform to saccular2. Partially or total thrombosis may be 
noted. 
Diffuse ground-glass opacity (GGO) (associated with diffuse alveolar hemorrhage 
[DAH]), focal or patchy areas of GGO or consolidation, cavitating and noncavitating 
nodules5. 
Poorly defined centrilobular small nodules (nodules <10 mm in diameter), and vascular 
tree-in-bud signs (small centrilobular nodules and nodular branching structures)5 
Sub pleural wedge shaped opacity may be noted in case of chronic pulmonary 
thromboembolism – s/o pulmonary infract. 
Thrombotic occlusion of the SVC with oedema of the mediastinal fat and multiple 
collateral vessels in the mediastinum and chest wall4. 
 
 
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Kumar et al.: MULTIPLE PULMONARY ARTERY ANEURYSMS : A CASE REPORT OF PULMONARY
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Therapeutic options  
Based on the Etiology the treatment varies. 
In case of vasculitis – Immunosuppressive therapy is the treatment of choice with close 
monitoring. 
In case of PAH, treatment should include calcium channel blockers, diuretics, and 
anticoagulants, and patients may benefit from the use of vasoactive substances such as 
endothelin receptor antagonists, phosphor-diesterase type 5 inhibitors, and prostacyclin 
derivatives2. 
Indications for surgical management are  
• Absolute PAA diameter ≥5.5 cm. 
• Increase in the diameter of the aneurysm of ≥0.5 cm in 6 months. 
• Compression of adjacent structures. 
• Thrombus formation in the aneurysm sack. 
• Evidence of valvular pathologies or shunt flow. 
 
Transcatheter embolization with steel coils is an effective and safe method of preventing 
aneurysm rupture1. 
Aneurysmorrhaphy. 
Aneurysmectomy and repair or replacement of the right ventricular outflow tract. 
 
 
 
 
 
Teaching points  
• Pulmonary vasculitis are non-infectious and are associated with granulomatous, 
eosinophilic, lymphoplasmocytic, or neutrophilic inflammatory diseases5. 
 
 
• Diseases of elastic arteries show aneurismal dilatation with or without intraluminal 
thrombosis or vascular stenosis with inflammatory wall thickening and luminal 
narrowing5. 
 
• Diseases of muscular arteries or arterioles usually manifest as cavitating or noncavitating 
nodules or multifocal consolidation along the bronchovascular bundles5. 
 
• Vasculitis involving capillaries or arterioles usually demonstrates DAH or small 
centrilobular nodules and tree-in-bud signs of vascular origin5. 
 
 
 
 
 
 
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References  
1. Pelage JP, El Hajjam M, Lagrange C, Chinet T, Vieillard-Baron A, Chagnon S, Lacombe P. 
Pulmonary artery interventions: an overview. Radiographics. 2005 Nov;25(6):1653-67. 
2. Kreibich M, Siepe M, Kroll J, Höhn R, Grohmann J, Beyersdorf F. Aneurysms of the 
pulmonary artery. Circulation. 2015 Jan 20;131(3):310-6. 
3. Castañer E, Alguersuari A, Gallardo X, Andreu M, Pallardó Y, Mata JM, Ramírez J. When to 
suspect pulmonary vasculitis: radiologic and clinical clues. Radiographics. 2010 Jan;30(1):33-
53. 
4. Seo JB, Im JG, Chung JW, Song JW, Goo JM, Park JH, Yeon KM. Pulmonary vasculitis: the 
spectrum of radiological findings. The British journal of radiology. 2000 Nov;73(875):1224-31. 
5. Chung MP, Yi CA, Lee HY, Han J, Lee KS. Imaging of pulmonary vasculitis. Radiology. 2010 
May;255(2):322-41. 
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MULTIPLE PULMONARY ARTERY ANEURYSMS : A CASE REPORT OF PULMONARY VASCULITIS

Sharath, Adiyuga

Digital Journal of Clinical Medicine 
Volume 3 Issue 3 Article 11 
1-1-2021 
Fibroid Uterus 
Adiyuga Sharath 
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 
Sharath, Adiyuga (2021) "Fibroid Uterus," Digital Journal of Clinical Medicine: Vol. 3: Iss. 3, Article 11. 
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. 
Fibroid Uterus 
Adiyuga Sharath , JSS Medical College, JSS AHER, Mysuru  
 
CLINICAL HISTORY: 
CLINICAL HISTORY 
A 36year old female patient came to the clinic with complaint of enlargement of abdomen for 
2 weeks and a sudden increase in weight from 60 kgs to 65.7 kgs in 2 weeks. 
MENSTRUAL HISTORY  
▪ Normal menstrual cycle  
▪ No dysmenorrhea  
▪ No menorrhagia  
▪ No clots passed  
OBSTETRIC HISTORY  
▪ Obstetric score –   G2P2A0L2 – Both LSCS  
▪ Last Child – 14 years old 
▪ LMP – 6/11/20 
            21/10/20 
            7/9/20 
PAST HISTORY 
The patient has no significant past history 
No previous history of surgeries  
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Sharath: Fibroid Uterus
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She has no history of diabetes mellitus, hypertension, thyroid, respiratory, cardiac or 
connective tissue abnormalities  
 
EXAMINATION AND INVESTIGATIONS: 
General physical examination  
The female patient was conscious, alert, cooperative and was well nourished, moderately 
built was well oriented to time, place and person.  
▪ No Pallor  
▪ No Icterus 
▪ No Cyanosis 
▪ No Clubbing 
▪ No Lymphadenopathy 
▪ No Oedema  
▪ Blood pressure-110/80  
▪ Pulse – 85 beats / min  
SYSTEMIC EXAMINATION 
CVS – S1, S2 heard 
RS- B/L normal  
PER ABDOMEN  
On Inspection – No Bulge was seen 
On Palpation – Firm lump from pelvis till epigastrium was felt 
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DOI: –
Bowel sounds are normal 
P/V examination – NAD 
CNS – No FND 
LOWER ABDOMEN USG – 
 
USG revealed a large solid mass along the posterior uterine wall from the cervix to the 
epigastrium as described, ovarian in origin D/D large serosal uterine fibroid. 
Ultrasound of lower abdomen excluded ovarian tumor  
 
FINAL DIAGNOSIS: 
Fibroid uterus  
Differential diagnosis  
Ovarian tumour  
Endometrial cancer   
Endometriosis  
 
DISCUSSION:  
Treatment:  
Patient underwent myomectomy under spinal anesthesia  
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Pre Surgery 
 
Fibroid 
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DOI: –
 
Fibroid with uterus 
 
Uterus with fallopian tube and ovaries 
Uterine leiomyomas (fibroids or myomas) are benign tumors of the uterus and clinically 
apparent in a large part of reproductive aged women. 
Clinically, they present with a variety of symptoms:  
▪  excessive menstrual bleeding, 
▪  dysmenorrhoea and intermenstrual bleeding 
▪  chronic pelvic pain 
▪  pressure symptoms such as a sensation of bloatedness, 
▪  increased urinary frequency 
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▪  bowel disturbance 
In addition, they may compromise reproductive functions, 
▪  possibly contributing to subfertility 
▪  early pregnancy loss 
▪  later pregnancy complications.[1] 
Treatment 
▪ Women with asymptomatic fibroids should be reassured that there is no evidence to 
substantiate major concern about malignancy and that hysterectomy is not indicated.  
▪ Treatment of women with uterine leiomyomas must be individualized based on 
symptomatology, size and location of fibroids, age, need and desire of the patient to 
preserve fertility or the uterus, the availability of therapy, and the experience of the 
therapist.  
▪ In women who do not wish to preserve fertility and/or their uterus and who have been 
counselled regarding the alternatives and risks, hysterectomy by the least invasive 
approach possible may be offered as the definitive treatment for symptomatic uterine 
fibroids and is associated with a high level of satisfaction.  
▪ Hysteroscopic myomectomy should be considered first-line conservative surgical 
therapy for the management of symptomatic intracavitary fibroids.  
▪ Surgical planning for myomectomy should be based on mapping the location, size, 
and number of fibroids with the help of appropriate imaging.  
▪ When morcellation is necessary to remove the specimen, the patient should be 
informed about possible risks and complications, including the fact that in rare cases 
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DOI: –
fibroid(s) may contain unexpected malignancy and that laparoscopic power 
morcellation may spread the cancer, potentially worsening their prognosis.  
▪ Anemia should be corrected prior to proceeding with elective surgery. (II-2A) 
Selective progesterone receptor modulators and gonadotropin-releasing hormone 
analogues are effective at correcting anemia and should be considered preoperatively 
in anemic patients.  
▪ Use of vasopressin, bupivacaine and epinephrine, misoprostol, peri-cervical 
tourniquet, or gelatin-thrombin matrix reduce blood loss at myomectomy and should 
be considered.  
▪ Uterine artery occlusion by embolization or surgical methods may be offered to 
selected women with symptomatic uterine fibroids who wish to preserve their uterus. 
Women choosing uterine artery occlusion for the treatment of fibroids should be 
counselled regarding possible risks, including the likelihood that fecundity and 
pregnancy may be impacted.  
▪ In women who present with acute uterine bleeding associated with uterine fibroids, 
conservative management with estrogens, selective progesterone receptor modulators, 
antifibrinolytics, Foley catheter tamponade, and/or operative hysteroscopic 
intervention may be considered, but hysterectomy may become necessary in some 
cases. In centres where available, intervention by uterine artery embolization may be 
considered.[2] 
Attempts at a nonsurgical treatment of uterine leiomyomas probably began hundreds of years 
ago, but scientifically validated modalities became available only some 40 years ago.During 
this relatively short period of time, several regimens were introduced using different 
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categories of drugs. Today, the most promising belong to two categories: PR modulators and 
orally active GnRHR blockers.[3] 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
1. Andrea Ciavattini, Jacopo Di Giuseppe, Piergiorgio Stortoni, Nina Montik, Stefano R. 
Giannubilo, Pietro Litta, Md. Soriful Islam, Andrea L. Tranquilli, Fernando M. Reis, 
Pasquapina Ciarmela, “Uterine Fibroids: Pathogenesis and Interactions with 
Endometrium and Endomyometrial Junction”, Obstetrics and Gynecology 
International, vol. 2013, Article ID 173184, 11 pages, 
2013. https://doi.org/10.1155/2013/173184 
2. Vilos GA, Allaire C, Laberge PY, Leyland N; SPECIAL CONTRIBUTORS. The 
management of uterine leiomyomas. J Obstet Gynaecol Can. 2015 Feb;37(2):157-178. 
doi: 10.1016/S1701-2163(15)30338-8. PMID: 25767949. 
3. Farris M, Bastianelli C, Rosato E, Brosens I, Benagiano G. Uterine fibroids: an update 
on current and emerging medical treatment options. Ther Clin Risk Manag. 
2019;15:157-178. https://doi.org/10.2147/TCRM.S147318 
 
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DOI: –


Fibroid Uterus

Tyagi, Dr. Anshika

Vasan, Dr. Col.T.S.

Digital Journal of Clinical Medicine 
Volume 3 Issue 1 Article 7 
1-1-2021 
Aplasia Cutis Congenital of Scalp With Right Parietal 
Encephalocele- A Rare Association With Surgical Apropos 
Dr. Anshika Tyagi 
JSS AHER 
Dr. Col.T.S. Vasan 
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 
Tyagi, Dr. Anshika and Vasan, Dr. Col.T.S. (2021) "Aplasia Cutis Congenital of Scalp With Right Parietal 
Encephalocele- A Rare Association With Surgical Apropos," Digital Journal of Clinical Medicine: Vol. 3: Iss. 
1, 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. 
Aplasia Cutis Congenital of Scalp With Right Parietal Encephalocele- A Rare 
Association With Surgical Apropos 
 Dr. AnshikaTyagi,  
Dr. Col.T.S.Vasan, Professor and Head, Department of Neuro Surgery, JSS Medical College, 
JSS AHER 
 
CLINICAL HISTORY: 
A 3.5-month-old male baby was brought with complaints of swelling on the right side of the 
head which was noticed by the mother at birth. It was associated with the watery discharge 
with a gaping scalp wound. 
PAST HISTORY 
The patient was a 3.5-month-old, male child delivered at 39weeks of gestation by LSCS. 
The child was previously operated on postnatal day 15 at a private hospital for complaints of 
well-demarcated right parietal scalp defect measuring 3x1cm with watery discharge and with 
surrounding hypoplastic scalp rim with the absence of hair. There was no fever or neck 
rigidity. 
It was diagnosed as APLASIA CUTIS CONGENITAL of the scalp and was managed with 
the closure of the defect with sutures. 
However, at 3.5 month of age, the child was taken to a private hospital for infected scalp post 
aplasia cutis, CSF leak & left upper limb focal seizures. There the baby underwent 
debridement with suturing  for the same. The gaping wound was poorly managed by simple 
sutures of the scalp & the child was referred to a higher centre by the surgeon. Later the baby 
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was admitted to our hospital on 07/10/2020 due to increasing size of swelling with watery 
discharge and gaping wound margins. 
The mother’s obstetrical records revealed no exposure to teratogens or febrile episodes. 
Except for the anomaly scan there were no other tests done for chromosomal anomalies. 
 
 
EXAMINATION AND INVESTIGATIONS: 
The baby was conscious, active, alert & was feeding well. Moved all 4 limbs. 
LOCAL EXAMINATION 
On local examination, there was an infected swelling in the right parietal scalp region just 
adjacent to the posterior fontanelle measuring 4 x 3 cm, translucent with overlying 
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granulation tissue. There were loose sutures from previous surgery in the gaping wound 
edges with watery discharge from the swelling. The swelling was almost reaching the midline 
and was surrounded by palpable bone anterolaterally and posterior fontanelle medially with 
an underlying stellate-shaped defect of the skull.  
OTHER SYSTEMS 
Respiratory System-B/L NVBS, No added sounds 
CVS-S1, S2+, No murmurs 
CNS-No focal neurological deficits. 
Per abdomen-Soft, Non-tender 
 
CT(Plain)-Gross widening of the sagittal suture, bregma, and adjacent coronal suture with 
herniation of right parietal lobe in extra-axial space. 
Herniated brain shows gliotic changes. 
Imp: Right parietal encephalocele. 
 
MRI-Gross diastasis of the sagittal suture with right high parietal encephalocele. 
Numerous small gyri along the inner cortex of the right frontal lobe with dilatation of extra-
axial spaces adjacent to it with Polymicrogyria. The rest of the right holo-hemisphere 
&lateral ventricle is mildly displaced superiorly. Myelination is normal for age.  
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BLOOD INVESTIGATIONS:- 
RBC-3.39mn/cumm 
MCV-84.7FL 
MCH-31.7gm/dl 
TLC-16460 cells/cumm 
PLATELET COUNT-6.36Lakh/cumm 
 
 
 
FINAL DIAGNOSIS:  APLASIA CUTIS CONGENITA OF SCALP WITH RIGHT 
PARIETAL ENCEPHALOCOELE 
DIFFERENTIAL DIAGNOSIS: - 
-Right parietal encephalocele 
-Cystic hygroma 
-Epidermal scalp cyst 
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DISCUSSION:  
Aplasia cutis congenital (ACC) is an uncommon condition with an estimated incidence of 3 
in 10000 births with only about 600 reported cases to date (1). ACC is characterized by the 
congenital absence of variant layers of scalp- epidermis, and dermis and in some cases bone 
& dura involving the vertex. It is known to be associated with limb and cardiac anomalies 
and rarely with meningoencephalocele. Common aetiological factors are epidermolysis 
bullosa in the mother, chromosomal abnormalities, teratogens & intrauterine infections( 2). 
Here we describe a case of ACC with right parietal encephalocele managed surgically with 
autologous fascia lata augmented duraplasty with tempero-occipital rotation scalp flap.ACC 
is a rare heterogeneous disorder with unknown pathogenesis. It is hypothesized to be due to 
developmental embryonic errors with incomplete closure of the outermost ectodermal portion 
of the neural tube(3). Other aetiological associations are epidermolysis bullosa, specific 
teratogens (methimazole and carbimazole), intrauterine infections, placental infarcts, 
chromosomal abnormalities & ectodermal dysplasias. This defect is usually covered by an 
ulcer or a thin membrane(4). 
The child was evaluated clinically and radiologically at our center. The other authors have 
recommended CT head with 3D reconstruction, MRI head, MR venography and angiography, 
complete sonographic evaluation (ocular, cerebral, cardiac, abdomino genital), and X-ray of 
limbs (4). 
Our aim of treatment was to achieve complete closure of the dural defect and hence avoid 
meningitis, bleeding, secondary local infection, and progressive brain damage. Earlier several 
authors have advocated conservative management to avoid operation and associated risks (2). 
The size of the lesion and underlying skull defect are the criteria universally accepted 
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Tyagi and Vasan: Aplasia Cutis Congenital of Scalp With Right Parietal Encephaloce
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favoring the surgical approach (2,5). Lesions around critical areas such as sagittal sinus have 
increased chances of bleeding and infection which also favor surgical intervention. Other 
known complications are seizures due to electrolyte imbalance, nutritional deficiency from 
chronic blood loss. There are various surgical procedures which include excision and wound 
closure, skin grafting, local scalp flaps with or without tissue expansion, free flaps, 
musculocutaneous flaps, full-thickness or split-thickness skin graft, and cranial vault 
reconstruction. In our case, the dural defect was almost reaching the midline with only a 2mm 
rim of the dura adjacent to the right lateral border of the superior sagittal sinus. The 
autologous fascia lata graft was meticulously sutured to cover the dural defect. We did not 
close the associated skull defect as the child was only 4 months old and according to 
literature, a bone defect can regenerate or can be repaired as delayed cranioplasty(1). By 
surgical intervention we effectively avoided the major complications resulting from CSF leak 
with an exposed brain, bleeding from superior sagittal sinus, and lessened chances of 
infection by providing adequate scalp cover to underlying vital structures. We advocate 
surgical management of ACC with encephalocele.(6)  
We would suggest complete syndromic evaluation of ACC and believe in an early surgical 
approach that minimizes complications and yet takes the advantage of innate regeneration 
ability of the newborn brain and the skull vault(7). This also highlights the need for referral 
of such children to specialized centers with sufficient experience and expertise(8). 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
 
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1. Alexandros B, Dimitrios G, Elias A, Evangelos D, Andreas M, Sotirios P, et al. 
Aplasia cutis congenita: Two case reports and discussion of the literature. Surg 
Neurol Int 2017;8:273. 
2. D. Ribuffo, M. Costantini, P. Gullo, N. D. Houseman & G. I. Taylor (2003) 
APLASIA CUTIS CONGENITA OF THE SCALP, THE SKULL, AND THE 
DURA, Scandinavian Journal of Plastic and Reconstructive Surgery and Hand 
Surgery, 37:3, 176-180. 
3. Rhee ST, Colville C, Buchman SR, Muraszko K. Complete osseous regeneration of a 
large skull defect in a patient with cutis aplasia: A conservative approach. J Craniofac 
Surg 2002;13:497-500 
4. Leboucq N, Montoya y Mártínez P, Montoya-Vigo F, Catan P. Aplasia cutis 
congenita of the scalp with large underlying skull defect: A case report. 
Neuroradiology 1994;36:480-2. 
5. Duan X, Yang G, Yu D, Yu C, Wang B, Guo Y. Aplasia cutis congenita: A case 
report and literature review. Exp Ther Med 2015;10:1893-95. 
6. Mahapatra AK. Management of encephalocoeles. Text Book of Operative 
Neurosurgery. New Delhi: BI Publications Pvt Ltd. 2005:279-90. 
7. Garland CB, Pomerantz JH. Regenerative strategies for craniofacial disorders. 
Frontiers in physiology. 2012 Dec 14;3:453. 
8. Opara PI, Ujuanbi AS, Okoro PE. Surgical admissions in a newborn unit in a low 
resource setting, challenges in management and outcomes. J Neonatal Biol. 
2014;3(2):132. 
 
 
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Aplasia Cutis Congenital of Scalp With Right Parietal Encephalocele- A Rare Association With Surgical Apropos

K P, Dr.Durkha Devi

M, Dr.Poornima

Digital Journal of Clinical Medicine 
Volume 3 Issue 3 Article 12 
1-1-2021 
A Case of Ovarian Torsion 
Dr.Durkha Devi K P 
JSS AHER 
Dr.Poornima 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 
K P, Dr.Durkha Devi and M, Dr.Poornima (2021) "A Case of Ovarian Torsion," Digital Journal of Clinical 
Medicine: Vol. 3: Iss. 3, Article 12. 
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 Ovarian Torsion 
 
Dr.Durkha Devi K P, Dr.Poornima M Department Of OBG, JSS Medical College, JSSAHER, 
Mysuru 
 
CLINICAL HISTORY: 
CLINICAL HISTORY 
A 28-year-old female presented with- 
Complaints of pain abdomen since a day, localized to the right lower abdomen, sudden in  
onset, intermittent, dullaching in character, non-radiating, relieving to some extent with  
analgesics with no aggravating factors. 
Associated with 2 episodes of vomiting, vomitus was non bilious, non-blood tinged and non- 
projectile. 
Her Urine pregnancy test is negative. 
Negative history: 
No history of trauma/fever/abdominal distension/jaundice/painful micturition/burning 
micturition. 
No history of bleeding per vagina/post coital bleeding/mass per vagina. 
No known co-morbidities/no known drug allergies/no history of surgeries in the past. 
Menstrual history: 
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LMP- 28/05/2019, Her last childbirth was 10 months back. 
Lactational amenorrhea is present. 
Previous cycles: 3-5 days/30-45 days, irregular, moderate flow, not associated with pain or 
clots. 
She was diagnosed with polycystic ovarian disease 6 years back and had undergone 
treatment  
for the same. 
Obstetric history: 
Obstetric score: Para 1 living 1 
Married life: 6 years of non-consanguinous marriage 
First pregnancy- conceived following ovulation induction, female baby delivered by FTND  
with birth weight of 3 kg, at present 9 months old, alive and healthy. 
EXAMINATION AND INVESTIGATIONS: 
CLINICAL EXAMINATION 
General physical examination: 
A young female patient moderately built and nourished, conscious, cooperative and well  
oriented to time, place and person. 
No pallor 
No icterus 
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No cyanosis 
No clubbing 
No lymphadenopathy 
No pedal oedema 
VITALS 
Temperature – Afebrile (98.4 F) 
Pulse rate – 80 beats per minute 
BP – 130/80 mm of Hg 
RR – 16 cycles per minute 
Systemic examination : 
CVS : S1, S2 heard, no murmurs. 
RS : Bilateral normal vesicular breath sounds heard. No added sounds. 
PER ABDOMEN : Soft, Tenderness present in hypogastric region and right iliac fossa + 
                                No organomegaly, Bowel sounds present. 
PER SPECULUM : Minimal white discharge present + 
PER VAGINA : Uterus anteverted, normal size, regular, mobile. 
                            Fullness present in Right fornix and posterior fornix. 
                            Tenderness present over right fornix. 
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Hb –  11.6 gm/dl 
PCV- 33.7 % 
RBC- 3.86 million/cumm 
MCH- 30.1 pg 
MCHC- 34.4 gm/dl 
MCV- 87.3 fl 
RDW- 11.9 % 
TLC – 13920 cells/cumm 
DLC –  
Neutrophils – 87.2 % 
Lymphocytes – 10.2 % 
Eosinophils – 0 % 
Basophils – 0.2 % 
Monocytes – 2.4 % 
Platelet – 2.88 lakhs/cumm 
PT – 12.5 seconds 
INR – 0.94 
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APTT – 25.4 seconds 
ULTRASOUND ABDOMEN AND PELVIS showed 
▪ Bulky (4.6 x 7.6 cm) and heteroechoic right ovary with peripherally arranged  
follicles and absent intrinsic vascularity. 
▪ Significant free fluid noted in pouch of douglas. 
▪ Fatty liver. 
 
FINAL DIAGNOSIS: 
28-YEAR-OLD PARA 1 LIVING 1 WITH RIGHT  OVARIAN TORSION 
DIFFERENTIAL DIAGNOSIS 
1. Ovarian torsion 
2. Tubo-ovarian abscess 
3. Ruptured Ectopic pregnancy 
4. Appendicitis 
5. Renal Calculi/Ureteric calculi 
6. Pelvic Inflammatory Disease 
 
DISCUSSION:  
Emergency Laparotomy was performed and following findings were noted. 
Per-operative findings : 
Hemoperitoneum of about 100ml noted. 
Right sided fallopian tube and ovary torsion (twisted thrice along its axis) noted. 
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Right ovary measuring about 5 x 7 cm with bosselated outer surface, dark brown to 
haemorrhagic in appearance was noted. 
Left ovary and fallopian tube normal, Uterus normal. 
RIGHT SALPINGO-OOPHORECTOMY WAS DONE. 
Right ovary and fallopian tube sent for HPE  revealed features consistent with ovarian torsion 
(no viable tissue) and hematosalpinx. 
 
 
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Ovarian torsion is a gynecological emergency which affects females of all age groups. It 
refers to the axial rotation of ovary on its ligamentous supports which compromises the 
vascular supply causing ischemic changes in the ovary. Higher incidence is seen in 
reproductive age group when compared to premenarchal and postmenopausal age groups 
(1).  Adnexal torsions usually involve both ovary and fallopian tube however there are fewer 
cases of isolated torsion involving either one (one in 1.5 million women) (1). Right ovary is 
slightly more prone to torsion because of relatively longer infundibulopelvic ligament on the 
right and also presence of descending colon on left side which supports left ovary preventing 
torsion. 
The predisposing factors for ovarian torsion include trauma, violent physical movements, 
contractions of pregnant uterus, intestinal peristalsis (7). The two common pathology which 
predisposes for torsion are  presence of  ovarian mass and  hypermobility of ovary, the former 
being more common. However, in paediatric and adolescent age group, ovarian torsion is 
associated with a normal ovary in about 46% of the cases (4). The predisposing factors in 
them include congenitally long ovarian ligaments, excessive laxity of pelvic ligaments, or a 
small uterus which allows more space for adnexa to twist on its axis (3).  
In adults, the most common underlying pathology is presence of an ovarian mass. More 
than  80% patients with ovarian torsion had an ovarian mass of 5cm or larger (1). The 
incidence of ovarian torsion with malignant tumours(<2%) is less than with benign tumours 
in reported case series (1).It is more common in dermoid or serous cystadenoma 
(7).Malignant tumors and endometriomas of ovary are prone to adhesions which prevent 
torsion in them. 
The other causes include PCOS (bulky ovaries),ovulation induction which may result in 
multiple large ovarian follicular cysts carrying increased risk of torsion (2).  
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The clinical features include acute onset of abdominal pain which is intermittent or sustained, 
nausea and vomiting, fever. Clinical examination findings may include a tender abdomen/ 
mass per abdomen. Pelvic examination reveals the mass per abdomen felt is separate from the 
uterus. 
Blood investigations may reveal a raised TLC or raised ESR in case of infection, increased 
specific tumour markers in case of suspected underlying tumors. However, imaging studies 
remain more relevant in diagnosing adnexal torsions. 
Pelvic ultrasonography is the imaging modality of choice. It has a 92% sensitivity and 96% 
specificity in detecting ovarian torsion (5). If USG shows normal ovary/adnexa,CT scan is 
used to rule out torsion. MRI is not recommended since urgent imaging is required if torsion 
is suspected. 
 USG findings suggestive of torsion include ovarian enlargement, hyperechogenic ovary with 
peripherally displaced follicles, free fluid in pouch of douglas and a coiled vascular pedicle 
which is commonly referred to as the whirlpool sign (6). Based on Doppler flow analysis of 
the ovary, the severity of adnexal torsion are graded as Class 1- coiling with arterial and 
venous blood flow, Class 2- coiling with arterial ovarian flow but no venous flow and Class 
3- true strangulation with no ovarian blood flow (8). However, normal Doppler study does 
not rule out the possibility of torsion owing to the dual blood supply of ovaries. 
Surgery is the gold standard treatment. Emergency Laparotomy/Laparoscopy is performed 
which is also the only way to confirm the diagnosis of torsion. The mainstay of  surgery is to 
assess the viability of ovary and its preservation. De-torsion which refers to the untwisting 
of  the axial rotation is the conservative procedure. Following de-torsion,  about 80% of the 
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patients had a normal follicular development (1). Salpingo-oophorectomy is the definitive 
surgery in cases of necrosed /gangrenous ovary. 
Oophoropexy (fixation of the ovary) is the treatment of choice in patients with increased 
chances of recurrence and patients with unilateral ovary. Various approaches of oophoropexy 
include fixation of ovary to either pelvic side wall, posterior abdominal wall or posterior wall 
of the uterus. Oophoropexy combined with shortening of the utero-ovarian ligament might be 
more efficacious in preventing recurrence (9). 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
1)Huang C, Hong MK, Ding DC. A review of ovary torsion. Ci Ji Yi Xue Za Zhi. 
2017:29(3):143-147. Doi:10.4103/tcmj_55_17 
2)Gorkemli h, Camus M, Clasen K. Adnexal torsion after gonadotropin ovulation induction 
for IVF or ICSI and its conservative treatment. Arch Gynecol Obstet. 2002:267:4-6. 
3)Kives S, Gascon S, Dubuc É, Van Eyk N. No. 341-Diagnosis and Management of Adnexal 
Torsion in Children, Adolescents, and Adults. J Obstet Gynaecol Can. 2017 Feb;39(2):82-90. 
doi: 10.1016/j.jogc.2016.10.001. PMID: 28241927. 
4) Sasaki KJ, Miller CE. Adnexal torsion: review of the literature. J Minim Invasive Gynecol 
2014:21:196-202. 
5) Bronstein ME, Pandya S, Snyder CW, Shi Q, Muensterer OJ. A meta-analysis of B-mode 
ultrasound, Doppler ultrasound, and computed tomography to diagnose pediatric ovarian 
torsion. Eur J Pediatr Surg 2015:25:82-6. 
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6) Feng JL, Lei T, Xie Hn, Li LJ, Du L. Spectrums and outcomes of adnexal torsion at 
different ages. J Ultrasound Med 2017:36:1859-66. 
7) Hiralal Konar, DC Dutta’s Textbook of Gynecology,6th Edition, 2013, Pages 298-299 
8) Auslender R, Shen O, Kaufman Y, Goldberg Y, Bardicef M, Lissak A, Lavie O. Doppler 
and gray-scale sonographic classification of adnexal torsion. Ultrasound Obstet Gynecol. 
2009 Aug;34(2):208-11. Doi: 10.1002/uog.6369. PMID:19606463. 
9) J.Hartley, M.Akhtar, and E.Edi-Osagie, “Oophoropexy for recurrent ovarian torsion,” Case 
Reports in Obstetrics and Gynecology, vol.2018, Article ID 8784958,4 pages,2018. 
 
 
 
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