Research Connect

Gupta, Dr. Tamanna

Pereira, Dr. Pratibha

Digital Journal of Clinical Medicine 
Volume 2 Issue 4 Article 9 
1-1-2020 
A Rare Cause of Hyponatremia 
Dr. Tamanna Gupta 
JSS AHER 
Dr. Pratibha Pereira 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
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Recommended Citation 
Gupta, Dr. Tamanna and Pereira, Dr. Pratibha (2020) "A Rare Cause of Hyponatremia," Digital Journal of 
Clinical Medicine: Vol. 2: Iss. 4, 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 Rare Cause of Hyponatremia 
 
 Dr. Tamanna Gupta, Dr. Pratibha Pereira  
 
CLINICAL HISTORY: 
Complains of vomiting since 1 day 
C/o hiccups since 1 day 
Known case of Hypertension (TAB TELMISARTAN 20MG 1-0-0) 
K/c/o Type 2 Diabetes  
Mellitus (Insulin Inj. Human Mixtard 30/70 20-0-16 U S/C) 
K/c/o Cerebrovascular accident (CVA) 
K/c/o Benign prostatic hyperplasia (BPH) 
K/c/o Coronary artery disease (CAD)- Triple vessel disease (Ecospirin Gold 0-0-1) 
 
EXAMINATION AND INVESTIGATIONS: 
 
BP: 140/80 mmHg  
RS: Bilateral NVBS, no added sounds 
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CVS: S1 S2 heard, no Murmurs 
Per Abdomen: Soft, Non-tender, No organomegaly. Bowel sounds heard. 
CNS Examination: Conscious, oriented, no focal neurological deficits. 
Blood routine, LFT, RFT, CXR, MRI brain were normal 
Urine Routine: 
1+ albuminuria 
2% sugar 
no ketone bodies 
Urea:27 
Creatinine:0.7 
Serum electrolytes: 
Na+ 122 
K+     5.6 
Cl-     96 
Glucose Random:286mg/dl 
Urine osmolality:364mOsm/kg water 
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USG abdomen: s/o BPH 
ECHO and Coronary angiogram: s/o CAD 
CT abdomen: Mild wall thickening involving pylorus and D1 segment of duodenum, Gall 
bladder sludge, small right renal calculi 
Upper GI endoscopy: Hiatus hernia, duodenal nodule(D1)-biopsy was taken-S/o neuroendocrine 
tumour 
ChromograninA:524.90ng/ml 
Serum gastrin: 171pg/ml 
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CT SCAN - ABDOMEN 
 
FINAL DIAGNOSIS: 
1.Duodenal Neuroendocrine tumor with Syndrome of inappropriate antidiuretic hormone 
secretion (SIADH) 
2.Hypertensive diabetic nephropathy 
3.Obstructive nephropathy 
4.Gastritis 
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TREATMENT: 
Tolvaptan was started and patient was followed for one month. 
Sodium correction was done. 
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DISCUSSION: 
This is a case of SIADH with no identifiable cause. Nevertheless, we incidentally found this 
patient to have functional Neuroendocrine tumour (NET) of the GIT. They can arise from any 
part of GIT. In relation to their pluripotent neuroendocrine cellular origin, NET can produce 
several resultant paraneoplastic syndromes. One of these syndromes is SIADH.  We associate 
this SIADH with NET. 
However, literature does not mention NET as one of the causes of SIADH. Persistent hiccups 
were an unusual presenting manifestation of hyponatremia.Tolvaptan selectively inhibits the 
binding of ADH to the V2 receptor . Binding to the V2 receptor induces excretion of electrolyte-
free water without altering the electrolyte excretion. 
ACKNOWLEDGEMENTS: None 
 
REFERENCES:  
1. J Emerg Med 1987 Jul-Aug;5(4):283-7 
2. Ecancermedicalscience. 2014 Jul 31;8:450. doi: 10.3332/ecancer.2014.450.eCollection 2014. 
3. https://pubmed.ncbi.nlm.nih.gov/8664818/ 
 
 
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English

A Rare Cause of Hyponatremia

G, Dr. Shivangi

Ravi, Dr. M.D.

Digital Journal of Clinical Medicine 
Volume 2 Issue 5 Article 8 
1-1-2020 
A Case Of Spina Bifida Occulta With Tethered Cord Syndrome 
Dr. Shivangi G 
JSS AHER 
Dr. M.D. Ravi 
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 
G, Dr. Shivangi and Ravi, Dr. M.D. (2020) "A Case Of Spina Bifida Occulta With Tethered Cord Syndrome," 
Digital Journal of Clinical Medicine: Vol. 2: Iss. 5, 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 Spina Bifida Occulta With Tethered Cord Syndrome 
Dr. Shivangi G.,7TH term MBBS 
Dr. M.D. Ravi, Professor, Department Of Pediatrics, JSS Medical College, JSS AHER, 
Mysuru  
Clinical History 
A 10-month-old baby presented with complaints of a lesion on the lower back since birth. 
The lesion was initially pinkish in color, present in the midline, 1×1.1 cm, irregular in shape, 
flat, and gradually changed color (presently brown). Puckering was present over the lesion. 
No h/o increase in size or depth of the lesion/seizures/bowel or bladder dysfunction/increase 
in the size of the head. 
It was initially diagnosed as a mole at a local medical facility and medications for local 
applications were prescribed. Recently, a discrepancy in lower limb length was noticed (left 
less than right) and Spina bifida occulta with a tethered cord was suspected and was admitted 
now for radiological investigations and further management. 
PAST HISTORY: H/o fever + 20 days before admission. No h/o prior hospitalization, No h/o 
seizure activity or involuntary movements 
ANTENATAL HISTORY: Mother did not take Folic Acid supplements during the first 
trimester of pregnancy. No h/o GDM/Gestational Hypertension/Thyroid disorder in the 
mother. 
NATAL HISTORY: Baby was born by Full Term LSCS due to the non-progression of 
labour. Birth weight – 3.1 kg. The baby cried immediately after birth. Feeds were initiated 
within 2 hours of delivery and there was no difficulty noted. No NICU admissions. 
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POSTNATAL HISTORY: Baby passed urine and meconium within 24 hrs. Uneventful 
postnatal period. 
DEVELOPMENTAL HISTORY: Baby has attained all milestones according to age. No 
developmental delay was noted. 
IMMUNISATION HISTORY: Immunisation is completed as per schedule. BCG, DPT-1, 
OPV-0, HiB, HepB has been given.  
NUTRITION HISTORY: The baby was exclusively breastfed for 6 months and weaning 
started with Ragi along with breastfeeds (4-5 times/day) 
The baby’s diet has mild deficiency of calories and proteins. 
FAMILY HISTORY: Secondborn of two children of a non-consanguinous marriage. No 
similar history in the family. No h/o congenital anomalies. 
The older child is an 8-year-old boy, alive and healthy. 
Examination 
A 10-month-old child is conscious, active, and alert. 
VITAL SIGNS:   
PR – 124 bpm 
RR – 24 CPM 
Temp.- 97.4°F 
SpO2- 96-97% at room air 
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CFT- <3 sec 
ANTHROPOMETRY  
  PRESENT EXPECTED PERCENTILE (WHO) 
WEIGHT 7.7 kg 9 kg 3rd-15th centile 
HEAD CIRCUMFERENCE 45 cm 44 cm 50th-85th centile 
LENGTH 72 cm 75 cm 15th-50th centile 
HEAD TO TOE EXAMINATION 
Normal. 
No icterus, no cyanosis, no edema, no lymphadenopathy 
SYSTEMIC EXAMINATION 
On CNS examination, the child was alert, conscious, and active. 
Neurological observation was significant for SACRAL DIMPLE, BROWNISH COLOUR, 
1×1.2 cm, IRREGULAR IN SHAPE, WITH DERMAL SINUS AND TUFT OF HAIR.  
Limb discrepancy + (left lower limb shorter than the right lower limb)  
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On palpation, a skeletal defect was noted along the region of the sacral spine. 
Cranial Nerves – B/L pupils reacting equally to light. No facial asymmetry. 
Motor system- Tone normal in all 4 limbs. Power 5/5 in all 4 limbs. 
                            The bulk of right thigh (22 cm) > Left thigh (21 cm) 
                            Length of left lower limb (31 cm) < right lower limb (32 cm) 
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Sensory system- could not be assessed 
No signs of meningeal irritation 
Musculoskeletal system normal 
CVS- S1, S2 heard. No murmurs. 
RS- Normal Vesicular breath sounds heard. No added sounds. 
PA- Soft, non-tender. 
 
Investigations 
Hb- 8.8 g/dL (normal 11-14 g/dL) 
TLC – 12,470 cells/cumm 
RBC – 3.75 million/cumm 
Platelets – 5.19 lakh/cumm 
LFT, RFT, Electrolytes – Within Normal Limits. 
MRI LUMBAR SPINE (under general anesthesia) –  
Well defined intradural lesion measuring 24x9x12 mm arising from filum terminale and seen 
extending from L4-S1 vertebrae. It is causing a mass effect on the Cauda Equina fibers 
displacing them anteriorly. Similar lesion is seen at the level of S2 vertebra measuring 3×3 
mm. ? MYXOPAPILLARY EPENDYMOMA 
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G and Ravi: A Case Of Spina Bifida Occulta With Tethered Cord Syndrome
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Intramedullary hyperintensity noted in the center of the spinal cord extending from L1-L2 
level measuring 20mm in length with a maximum thickness of 3 mm – SYRINX 
A linear hypointense tract measuring 1.5 mm in width is seen extending from the cutaneous 
plane at L4 level, descending antero-inferiorly, and terminating at the spinous process of the 
L5 vertebra. – DORSAL DERMAL SINUS 
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Diagnosis 
1. Spina Bifida Occulta with Tethered Cord Syndrome 
2.  ? Myxopapillary Ependymoma with Syrinx at L1-L2 with Dorsal Dermal Sinus at L4-L5 
3. ? Lipoma 
Treatment 
Plan for neurosurgical intervention through a midline vertical approach with intraoperative 
nerve monitoring, which would include – 
1. Excision of the dermal sinus tract 
2. L4-S2 laminectomy and excision of the space occupying lesion (? 
Lipoma/Myxopapillary ependymoma) 
3. Detethering of the cord. 
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G and Ravi: A Case Of Spina Bifida Occulta With Tethered Cord Syndrome
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Discussion 
The Neural tube is the structure in the developing embryo that eventually becomes the brain, 
spinal cord, and the tissues that enclose them. The neural tube forms early in pregnancy and 
closes by the 28th day after conception. [1] 
Neural tube defects are one of the most common congenital anomalies due to the failure of 
closure of the neural tube during embryogenesis. These defects can be open (exposed neural 
tissue), e.g. craniorachischisis, anencephaly; or closed (neural tissue covering intact), e.g. 
Encephalocele, Spina Bifida Occulta. [1] 
Specific folate deficiencies at the cellular level may be responsible for NTDs because of 
deranged bioavailability. There can be presence of autoantibodies binding the folate receptors 
and blocking cellular uptake of folates. [1,2]. 
Folates play a major role in nucleotide synthesis. Rapidly dividing cells of the neural tube in 
embryos require synthesis of a large number of nucleotides to allow DNA replication [1] and 
hence deficiency of folate during the first trimester of pregnancy has been implicated in the 
increased incidence of NTDs. 
Spina bifida, depending on the level of the lesion, can cause interruption of the spinal cord at 
that site- resulting in paralysis of lower limbs, bowel/bladder dysfunction, anesthesia of 
overlying skin, and abnormalities of hips, knees, and feet. [3] It is also commonly associated 
with hydrocephalus and Arnold Chiari malformation which cause an increase in  size of the 
head. 
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Spina Bifida Occulta is the failure of bony fusion of the vertebral column that is covered by 
skin, with or without an overlying tuft of hair, lipoma, or sinus. [4]  
Tethered cord syndrome (TCS) is a common association with Spina Bifida, as seen in the 
above-discussed case as well. It is a neurological disorder caused by tissue attachments that 
limit the movement of the spinal cord within the spinal column. These attachments can cause 
an abnormal stretching of the spinal cord. The magnitude and degree of traction govern the 
reversibility of cord dysfunction. 
Failure of regression of the caudal cell mass gives rise to a hypertrophic or fibrous filum 
terminale. Decreased viscoelasticity of a thickened or fatty filum places traction on the lower 
spinal cord, displacing the conus below the level of L2. TCS presents with cutaneous and 
neurological symptoms. [5] 
Cutaneous features (predominantly seen in neonates and infants): Dimples at the level of 
lumbar/upper sacral spine, hypertrichosis, hemangioma, dermal sinus, subcutaneous lipomas.  
Neurological features: Lower extremity weakness, muscle atrophy, sensory loss in the 
perineal region,  abnormal gait (toe walking, due to tight heel cords), Limb discrepancies. [5] 
Detethering is performed if clinical signs and symptoms of deterioration are present. 10-20% 
of children may require repeat surgeries for correction as symptoms of tethering may 
reappear during periods of growth. [6] 
Syrinx or Syringomyelia is the presence of fluid-filled cyst within the spinal cord, which may 
grow over time. When the syrinx is present in the distal third of the cord, it is called 
“Terminal Syringomyelia” and is often associated with tethered cord and spina bifida. [7] 
Radial tension on the spinal cord due to intermittent low pressure of the cord parenchyma 
may draw in interstitial fluid and result in enlargement of the syrinx. 
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MRI  is the gold standard for diagnosis and Syringomyelia is considered one of the most 
important radiological findings in cord tethering. 
Immediate surgical intervention is not necessitated unless the patient is symptomatic or the 
syrinx is extensive. [8] 
Ependymomas are rare tumors which take origin from the neuroectoderm and are classified 
as Grade I – myxopapillary ependymoma, subependymoma; Grade II ependymoma; Grade III 
– Anaplastic ependymoma [9] 
Myxopapillary Ependymoma is slow-growing, usually benign, and occurs in the lower part of 
the spinal column. They are known to recur locally and are treated with aggressive surgery, 
chemotherapy, radiation therapy. [10] 
 
 
References 
1. Apoline Imbard, Jean Francois Benoist, and Henk J. Blom. Neural Tube Defects, Folic 
Acid, and Methylation. Int J Environ Res Public Health, 2013 
2. Rothenberg S.P., da Costa M.P., Sequeira J.M., Cracco J., Roberts J.L., Weedon J., 
Quadros E.V. Autoantibodies against folate receptors in women with a pregnancy 
complicated by neural tube defect. N. Engl. J. Med. 2004 
3. H. Northrup et al. Spina Bifida and other neural tube defects. Curr Probl Pediatr. Nov-Dec 
2000. 
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4. Ghai, Vinod K Paul, Arvind Bagga. Essential pediatrics. 9th edition. CBS Publishers. New 
Delhi. 2019 
5. Yamada S, Zinke DE, Sanders D: Pathophysiology of “tethered cord syndrome”. J 
neurosurg 54: 494-503, 1981 
6. Omar Zalatimo. Tethered Spinal Cord Syndrome. American Association of Neurological 
Surgeons. 2020 
7.  Beaumont A, Muszynski CA, Kaufman BA. Clinical significance of terminal 
syringomyelia with pediatric tethered cord syndrome. Pediatr Neurosurg. 2007; 43:216–221 
8. Ji Yeoun Lee, Kyung Hyun Kim, Kyu-Chang Wang. J Korean Neurosurg Soc 2020 May; 
63(3):338-341 
9. Michele Reni et al. Crit Rev Oncol Hematol. 2007 Jul. 
10. Daniel R Fassett, Meic H. Schmidt. Lumbosacral Ependymomas: A review of the 
management of intradural and extradural tumors. Medscape Neurosurg Focus. 2003 
 
 
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A Case Of Spina Bifida Occulta With Tethered Cord Syndrome

Chintamaneni, Dr. Supritha

Prasad S, Dr.Rajendra

M, Dr.Bhanukumar

L S, Dr.Adarsh

Digital Journal of Clinical Medicine 
Volume 2 Issue 4 Article 10 
1-1-2020 
Tuberculoma presenting as Paradoxical IRIS in a HIV positive 
patient 
Dr. Supritha Chintamaneni 
JSS AHER 
Dr.Rajendra Prasad S 
JSS AHER 
Dr.Bhanukumar M 
JSS AHER 
Dr.Adarsh L S 
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 
Chintamaneni, Dr. Supritha; Prasad S, Dr.Rajendra; M, Dr.Bhanukumar; and L S, Dr.Adarsh (2020) 
"Tuberculoma presenting as Paradoxical IRIS in a HIV positive patient," Digital Journal of Clinical 
Medicine: Vol. 2: Iss. 4, 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. 
Tuberculoma presenting as Paradoxical IRIS in a HIV positive patient 
Dr. Supritha Chintamaneni, Dr.Rajendra Prasad S, Dr.Bhanukumar M, Dr.Adarsh L S, 
Dr.Nandini K  
 
CLINICAL HISTORY: 
A 38-year-old male patient hailing from Mysuru district came with complains of fever and 
headache of 3 days uration. He is a known case of RVD. 3 months back he was diagnosed to be 
having TBM along with CMV Retinitis. SF CBNAAT was positive. Fundoscopy showed 
features of CMV Retinitis. The patient was started on ATT according to RNTCP guidelines. 
Patient was also initiated on Valgancyclovir for CMV Retinitis. There was a significant 
improvement in patient’s condition.  
Patient was referred to ART centre for further management. Patient CD4 count was 12. ART was 
initiated after 3 onths of starting ATT. After 1 week of  starting ART, patient presented with the 
above symptoms. No H/O cough, breathlessness or Gastro Intesinal symptoms. 
EXAMINATION AND INVESTIGATIONS:  
A middle-aged man moderately built and nourished is alert, conscious and co-operative. Oriented 
to time, place and person.  No pallor/icterus/clubbing/cyanosis/lymphadenopathy/edema.Vitals 
stable. 
Central Nervous System:Higher mental function-Intact 
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Motor System-Normal Cranial Nerves 
Fundoscopy: Choroid tubercles noted in the superotemporal quadrants of both the eyes. 
Rest of the findings were normal.Bilateral pupil equally reactive No signs of cerebellar 
dysfunction 
No signs of meningeal irritation 
CVS:  S1S2 heard, no murmurs 
Respiratory System: B/L Normal vesicular breath sounds, no added sounds 
Per Abdomen: Soft, non-tender, no organomegaly 
Hb-13.6 gm/dl 
TLC-6310 cells/cumm 
Platelet-2.8 lakh/cumm 
Neutrophils-51% 
Lymphocytes-42.5% 
ESR-60mm in 1 Hr 
MRI Brain (plain+contrast) Multiple homogenously enhancing nodular lesions in the bilateral 
cerebral & cerebellar  
hemispheres, capsuloganglionic region of the thalamus, body of corpus callosum and brainstem. 
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FINAL DIAGNOSIS: 
The following differential diagnosis were considered in view of RVD status, low CD4 count and 
ring enhancing shadows in the MRI of the brain.  
a.Neurotoxoplasmosis     
b.Brain metastasis 
c.Neurocysticercosis     
d.Brain abscess 
e.Tuberculoma        
f.CNS Lymphoma 
Final diagnosis –  
TUBERCULOMA(PARADOXICAL IRIS) 
TREATMENT: 
Since the patient was a known case of Tuberculosis, a high probability of Tuberculosis was 
considered and ATT was continued. ART was also continued along with steroids. 
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-Anti Tubercular Treatment-Anti Retroviral Treatment- 
TAB.COTRIMOXAZOLE PO 1-0-0  
-TAB.DOLO 650mg PO 1-1-1– 
INJ DEXAMETHASONE 4mg IV 1-1-1 – 
Tab.VALGANCICLOVIR 450 mg 2-0-2 for 21 days and later 2-0-0 
 DISCHARGE TREATMENT:-Continue ATT-Continue ART-TAB.CO – TRIMOXAZOLE PO 
1-0-0-TAB.DEXAMETHASONE 0.4mg/kg/day for 6 weeks and gradually tapered- 
CAP. PANTOPRAZOLE 40 mg 1-0-0-Continue 
TAB. VALGANCICLOVIR 2-0-0 
DISCUSSION:  
The immune reconstitution inflammatory syndrome (IRIS; also known as immune reconstitution 
disease, 
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immune reconstitution syndrome, or immune restoration disease) is a widely recognized 
phenomenon that can complicate antiretroviral therapy (ART)[1,2]. The infectious pathogens 
most often seen in the syndrome are mycobacteria, varicella zoster, herpesviruses, and 
cytomegalovirus (CMV)[3]. 
There are two common IRIS presentations in HIV-infected persons that both occur in the first 
months after commencing ART which are paradoxical IRIS and unmasking IRIS[4,5]. In 
paradoxical tuberculosis-associated IRIS, patients are known cases of active TB and have shown 
improvement in their health condition upon initiation of ATT. Following initiation of ART, IRIS 
can present as recurrent, new, or worsening symptoms or signs of tuberculosis such as fever, 
return of cough, or lymph node enlargement, or recurrent, new, or deteriorating radiological 
manifestations. Risk factors include more advanced HIV disease with lower CD4 cell count, 
disseminated and extrapulmonary tuberculosis, a shorter delay between the start of tuberculosis 
treatment and initiation of ART (ideally 4– 6 weeks[6]), and a more vigorous immunological and 
virological response to ART[7]. 
 
It may manifest as meningitis, brain tuberculomas, brain abscesses, radiculomyelitis, and spinal 
epidural abscesses[8,9,10,11]. Unmasking IRIS occurs due to missed diagnosis of TB that can be 
seen in patients(highly immunocompromised) with inherent insensitivity of tuberculosis, an 
active subclinical disease at the time of ART initiation and presentation of symptomatic disease 
might result from ART-induced restoration of an immune response against Mycobacterium 
tuberculosis antigens that results in inflammation. [7]. 
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In both situations, the immune system is rapidly adapting from an inadequate response to an 
escalated inflammatory response toward the pathogen[4,5].The diagnostic approach to neuro-
TB-IRIS suspects should focus on the exclusion of other causes for worsening, such as poor 
adherence to TB drugs, drug reactions or toxicities, infection with a TB drug-resistant strain, and 
an uncommon or additional opportunistic etiology [7]. 
The management of IRIS is symptomatic. In case of TBM- IRIS,ATT and ART are continued 
and to reduce the inflammation steroids are started. The Choice of steroid is Dexamethasone. 
According to Thwaite study, Dexamethasone has a good anti -inflammatory effect and reduces 
the mortality, though has got minimal effect in 
preventing neurological disability[12]. 
REFERENCES: 
1.Hamill RJ. The immune reconstitution inflammatory syndrome. AIDS reviews. 2003;5(2):67-
79  
2.French MA, Price P, Stone SF. Immune restoration disease after antiretroviral therapy. Aids. 
2004 Aug 20;18(12):1615-27 
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3.Murdoch DM, Venter WD, Van Rie A, Feldman C. Immune reconstitution inflammatory 
syndrome (IRIS): review of common infectious manifestations and treatment options. AIDS 
research and therapy. 2007 Dec;4(1):1-0 
4.Rammohan KW, O’Connor PW, Ortega MR, Delgado SR, Tornes L. Disease activity return 
during natalizumab treatment interruption in patients with multiple sclerosisAuthor Response. 
Neurology. 2011 Nov 22;77(21):1930-1 
5.Narayanan S, Banerjee C, Holt PA. Cryptococcal immune reconstitution syndrome during 
steroid withdrawal treated with hydroxychloroquine. International Journal of Infectious Diseases. 
2011 Jan 1;15(1):e70-3  
6.Török ME, Yen NT, Chau TT, Mai NT, Phu NH, Mai PP, Dung NT, Chau NV, Bang ND, Tien 
NA, Minh NH. Timing of initiation of antiretroviral therapy in human immunodeficiency virus 
(HIV)–associated tuberculous meningitis. Clinical infectious diseases. 2011 Jun 1;52(11):1374-
83 
7.Meintjes G, Lawn SD, Scano F, Maartens G, French MA, Worodria W, Elliott JH, Murdoch D, 
Wilkinson RJ, Seyler C, John L. Tuberculosis-associated immune reconstitution inflammatory 
syndrome: case definitions for use in resource-limited settings. The Lancet infectious diseases. 
2008 Aug 1;8(8):516-23 
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8.Marais S, Meintjes G, Pepper DJ, Dodd LE, Schutz C, Ismail Z, Wilkinson KA, Wilkinson RJ. 
Frequency, severity, and prediction of tuberculous meningitis immune reconstitution 
inflammatory syndrome. Clinical infectious diseases. 2013 Feb 1;56(3):450-60 
9.Pepper DJ, Marais S, Maartens G, Rebe K, Morroni C, Rangaka MX, Oni T, Wilkinson RJ, 
Meintjes G. Neurologic manifestations of paradoxical tuberculosis-associated immune 
reconstitution inflammatory syndrome: a case series. Clinical Infectious Diseases. 2009 Jun 
1;48(11):e96-107 
10.Agarwal U, Kumar A, Behera D, French MA, Price P. Tuberculosis associated immune 
reconstitution inflammatory syndrome in patients infected with HIV: meningitis a potentially life 
threatening manifestation. AIDS research and therapy. 2012 Dec 1;9(1):17 
11.Vidal JE, Cimerman S, Schiavon Nogueira R, Bonasser Filho F, Sztajnbok J, Silva PR, Lins 
DL, Coelho JF. Paradoxical reaction during treatment of tuberculous brain abscess in a patient 
with AIDS. Revista do Instituto de Medicina Tropical de São Paulo. 2003 Jun;45(3):177-8 
12.Thwaites GE, Bang ND, Dung NH, Quy HT, Oanh DT, Thoa NT, Hien NQ, Thuc NT, Hai 
NN, Lan NT, Lan NN. Dexamethasone for the treatment of tuberculous meningitis in adolescents 
and adults. New England Journal of Medicine. 2004 Oct 21;351(17):1741-51 
 
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Tuberculoma presenting as Paradoxical IRIS in a HIV positive patient

Karkra, Rohan

Digital Journal of Clinical Medicine 
Volume 2 Issue 1 Article 7 
1-1-2020 
Kikuchi-Fujimoto Disease 
Rohan Karkra 
JSS AHER 
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 Part of the Dentistry Commons, Health Policy Commons, Medical Education Commons, Pharmacy 
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Recommended Citation 
Karkra, Rohan (2020) "Kikuchi-Fujimoto Disease," Digital Journal of Clinical Medicine: Vol. 2: 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. 
Kikuchi-Fujimoto Disease 
Rohan Karkra, JSS Medical College, JSS AHER  
 
CLINICAL HISTORY: 
A 25 year male patient came with the complaints fever with chills since 3 months. Fever was 
high grade, intermittent and showed evening rise of temperature 
He gives h/o myalgia, fatigue, loss of appetite and significant weight loss. 
No h/o of cough, rashes, abdominal pain, diarrhoea. 
Not a k/c/o diabetes mellitus, hypertension, thyroid disorders, cardiac disorders 
Past History: 
He was a k/c/o of kikuchi fujimoto disease, diagnosed 3 years back at same hospital. 
 
EXAMINATION AND INVESTIGATIONS: 
General Physical Examination: 
Febrile 
Pallor: present 
B/L cervical (posterior and anterior triangle), axillary, inguinal, and epitrochlear non-tender 
lymphadenopathy. 
Lymph nodes were soft and non-matted. 
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Systemic Examination: 
ABD: No organomegaly 
Normal bowel sounds. 
CVS: S1S2 heard. No murmurs 
RS: B/L NVBS. No added sounds. 
 
Blood Investigations:   Hb: 10.8 g% PCV: 32.4% MCHC: 33.3 g/dL TLC: 3510 
cells/cumm Platelets: 1.5 lakh/cumm PBS: Microcytic hypochromic anaemia with 
leukopenia.   
Malaria Card Test: Immunochromatographic test – negative   
Tuberculosis Test: Acid fast bacilli (AFB) staining negative.   
Paul Bunnell Test:   Negative for infectious mononucleosis   
Fine Needle Aspiration Cytology Reactive lymphadenitis with histiocytes, tingible 
body macrophages.   
Biopsy: Biopsy of scalene lymph node show no granulomas but areas of necrosis 
and signs of lymphadenitis 
  
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CT FINDINGS: 
2 enlarged lymph nodes showing necrotic foci and some perinodal infiltration (arrow head) 
 
 
FINAL DIAGNOSIS: 
1. Kikuchi Fujimoto Disease 
2. Tuberculosis 
3. Infectious Mononucleosis 
4. Systemic Lupus Erythematosus 
Treatment Given:  
TAB. PARACETAMOL 650 mg 1-1-1 PO 
TAB DEXAMETHASONE 4 mg 1-1-1 PO TILL SYMPTOMS PERSIST, THEN 
TAPERED OVER 1 WEEK 
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TAB PREDNISOLONE 20 mg 1-1-0 PO TILL SYMPTOMS PERSIST, THEN TAPERED 
OVER 1 WEEK 
TAB PANTOPRAZOLE 40 mg 1-0-0 PO 
INJ. PARACETAMOL 1gm i.v SOS 
 
DISCUSSION: 
Kikuchi Fujimoto is an extremely rare, sporadic and benign condition of unknown etiology 
which causes fever, necrotizing lymphadenopathy, rashes, headache and occasionally 
leukopenia[1]. The symptoms are usually self-limiting. The condition was first described in 
1972 in Japan as a new type of lymphadenitis with focal reticulum cell hyperplasia[2]. This 
condition is almost always found in young women[3]. Over a period of 15 years (1986-2000), 
only 330 cases were reported worldwide[4], in contrast to the period 1996-2012 in which only 
9 cases were reported[5]. This makes this case a particularly rare diagnosis. 
Kikuchi disease is often associated with Systemic Lupus Erythematosus and hence must be 
evaluated for the same using an antinuclear antibody profile. 
Clinically, the disease is often confused for tuberculosis and sarcoidosis due to similar 
presentation. 
Histologically, necrosis, karryorhectic debris, crescent shaped histiocytes and plasmacytoid 
monocytes can be seen. Treatment is mainly symptomatic and relies heavily on NSAIDs and 
corticosteroids. Death is unlikely and there is a 3% recurrence . 
ACKNOWLEDGEMENTS: None  
 
 
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REFERENCES 
1. Mahajan T, Merriman R, Stone M. Kikuchi-Fujimoto Disease (Histiocytic Necrotizing 
Lymphadenitis): Report of a Case with Other Autoimmune Manifestations. Baylor 
University Medical Center Proceedings. 2007;20(2):149-151. 
2. Archibald D, Carlson M, Gustafson R. Kikuchi-Fujimoto Disease in a 30-Year-Old 
Caucasian Female. International Journal of Otolaryngology. 2009;2009:1-4. 
3. Deaver D, Naghashpour M, Sokol L. Kikuchi-Fujimoto Disease in the United States: 
Three Case Reports and Review of the Literature. Mediterranean Journal of Hematology 
and Infectious Diseases. 2013;6(1):e2014001. 
4. Lin H. Kikuchi’s disease: a review and analysis of 61 cases. Otolaryngology – Head and 
Neck Surgery. 2003;128(5):650-653. 
5. Lee B, Patel R. Kikuchi–Fujimoto Disease. Clinical Pediatrics. 2012;52(1):92-95. 
6. Image 2 – https://en.wikipedia.org/wiki/Kikuchi_disease – Copyright © 2011 Michael 
Bonert 
7. Image 3 – Lee S, Yoo J, Lee S. Kikuchi Disease: Differentiation from Tuberculous 
Lymphadenitis Based on Patterns of Nodal Necrosis on CT. 2019. American Journal of 
Neuroradiology January 2012, 33 (1) 135-140; DOI: https://doi.org/10.3174/ajnr.A2724 
 
 
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Kikuchi-Fujimoto Disease

Bhargava, Vibhu

Barve, Dr. Sandeep

Digital Journal of Clinical Medicine 
Volume 2 Issue 1 Article 10 
1-1-2020 
Sickle Cell Disease 
Vibhu Bhargava 
DY Patil Medical College And Hospital & Research Centre 
Dr. Sandeep Barve 
Parul Institute Of Medical Sciences And Research 
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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 
Bhargava, Vibhu and Barve, Dr. Sandeep (2020) "Sickle Cell Disease," Digital Journal of Clinical Medicine: 
Vol. 2: Iss. 1, 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. 
Sickle Cell Disease 
Vibhu Bhargava, 4th Term, DY Patil Medical College And Hospital & 
Research Centre, Pimpri-Chinchwad, Maharastra ; Dr. Sandeep Barve, 
Professor Of Pathology, Parul Institute Of Medical Sciences And Research, 
Vadodara, Gujarat  
 
 
 
 
CLINICAL HISTORY: 
 
29 year old male patient came with the complaints of abdominal pain since 3 
months, insidious in onset, non-progressive. He also gives history of low grade 
fever and cough. Cough is associated with expectoration, whitish to yellowish 
in color, mild in quantity, not blood tinged, not foul smelling. History of 2-3 
episodes of vomiting since 1 week, non-bile tinged. 
No history of joint pain, breathlessness and fatigue. 
Past history: The patient is a known case of sickle cell disease diagnosed in 
childhood. 
He has undergone multiple blood transfusions since childhood. 
No history of diabetes mellitus, hypertension, thyroid disorders or cardiac 
disorders. 
 
EXAMINATION AND INVESTIGATIONS: 
 
General Physical Examination: 
Febrile. (99.2 F) 
Pallor and icterus present. 
No generalised lymphadenopathy. 
Systemic Examination: 
Abdomen: 
Inspection: Umbilicus central. No distention visible 
Palpation : 
Tenderness present in the epigastric region. Mild tenderness present in RUQ on 
deep palpation. 
Murphy’s sign negative. 
Percussion: Normal. No Signs of free fluid. 
Auscultation. Normal bowel sounds heard. 
CVS: S1, S2 heard.No murmurs. 
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RS: NVBS heard on the right side. Decreased breath sounds over the left lung. 
No added sounds. 
CNS: Normal. 
Blood Investigations: 
Hb:9.1gms/dl 
Total WBC: 
15,220/mcl 
N:71%, L:20% 
RBC:4.16 million/mcl 
MCV:69.8% 
MCH:21.9% 
MCHC:31.4% 
RDW-CV:17.5% 
Platelet:53000/mcl 
Peripheral Blood Smear: 
Red blood cells are normocytic normochromic to mildly hypochromic. 
Moderate degree of anisopoikilocytosis noted. 
Sickle cells seen. (Marked in black) 
(Insert Image 1) 
 
 
 
 
 
 
 
 
 
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Solubility Sickling Test: 
Positive 
(Insert Image 2) 
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1.  
Hb analysis by HPLC 
Hb A:9.8% 
Hb A2: 2.9% 
Hb F: 6.2% 
Hb S: 81.1% 
Findings are suggestive of SICKLE CELL SYNDROME. 
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1.  
(Insert Image 3) 
X-Ray Chest (PA view) 
Blunting of left costophrenic angle. s/o left pleural effusion. 
(Insert image 4) 
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1.  
MDCT Abdomen & Pelvis: 
Acute pancreatitis with intrapancreatic pseudocysts. 
Cholelithiasis. 
Left mild to moderate pleural effusion..  
    
FINAL DIAGNOSIS: 
 
SICKLE CELL DISEASE WITH PLEURAL EFFUSION AND 
CHOLELITHIASIS 
DISCUSSION: 
 
NJ CEFTRIAXONE 1 GM IV x 7 days   
TAB FOLVIT (Folic acid) x 5 days   
TAB PANTOPRAZOLE 1-0-1 X 20 days   
Pleural tapping was advised SOS.   
 
The patient refused further interventions, hereafter.   
 
 
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Sickle cell disease is a common hereditary hemoglobinopathy caused by a point 
mutation in B globin that promotes the polymerisation of deoxygenated 
haemoglobin leading to red cell distortion, microvascular obstruction, 
haemolytic anaemia and ischemic tissue damage.1 
The replacement of β6 glutamic acid with valine results in a hydrophobic 
interaction of sickle hemoglobin (hemoglobin S) with another hemoglobin 
molecule in conditions of low oxygen availability, trigger an aggregation into 
large polymers. The polymerization of deoxygenated hemoglobin S is the 
primary event in the molecular pathogenesis of sickle cell disease, resulting in a 
distortion of the shape of the red cell (banana or sickle shaped) and a marked 
decrease in its deformability. These rigid cells are responsible for the vaso-
occlusive phenomena that are the hallmark of the disease.2 
SCD is caused by genetic and non-genetic factors. The genetic cause is 
characterized by the presence of abnormal erythrocytes damaged by HbS, a 
variant of normal adult hemoglobin (HbA), inherited either from both parents 
(homozygous for the HbS gene) or with β-thalassemia (compound 
heterozygosity) or from one parent, along with another hemoglobin variant, 
such as hemoglobin C (HbC). The non-genetic factors include climate, air 
quality, as well as socioeconomic factors. 2,3 
Dactylitis is the most common initial symptom, noted in children in the first 2 
years of life whereas painful crisis is the first symptom frequently seen in 
patients after the age of 2 years. The most common nonspecific symptom is 
pneumonia.4 
Infection is a major determinant of the outcome in patients with sickle cell 
disease. Splenic dysfunction has a key role in the increased susceptibility to 
bacterial infections seen in children with sickle cell disease, and pneumococcal 
and haemophilus infections.3 
The complications of sickle cell disease are varied ranging from vaso-occlusive 
crisis to acute chest syndrome, and pulmonary hypertension.5 A dreaded 
complication of formation of silent infarcts due to adherence of sickle cells to 
the endothelium, causing activation of the inflammatory cascade and clotting 
factors resulting in in a nidus for thrombus formation can lead to severe motor 
and cognitive impairment.6 
Clinical outcomes have gradually improved over the years, mostly as a result of 
developments in supportive care and treatment with hydroxyurea, which 
stimulates hemoglobin F production.2 Penicillin prophylaxis in children, 
primary stroke prevention, regular blood transfusions are main modalities of 
treatment and prevention. 4 
Hematopoietic stem-cell transplantation is potentially curative, although its use 
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is restricted by the high cost, toxicity, and limited availability of suitable 
donors.3 
 
 
CONCLUSION: 
 
We reviewed a case of a 29-year male, adult who presented with acute pain 
abdomen and additional history of  low grade fever . This report illustrates the 
importance of  having valid differentials for pain abdomen in an acute setting  
and performing the required valid blood investigations.prompt treatment by 
medical line of management at diagnosis to improve outcome and prevent 
complications   recurrent infection and vaso occlusive complications. 
ACKNOWLEDGEMENTS:None  
 
1. REFERENCES: Robbins S, Cotran R,Kumar V, Abbas A, Aster J. Pathologic 
basis of disease. Philadelphia, PA: Saunders Elsevier; 2015. 
2. Bunn H. Pathogenesis and Treatment of Sickle Cell Disease. New England 
Journal of Medicine. 1997;337(11):762-769. 
3. Piel, F., Steinberg, M. and Rees, D. (2017). Sickle Cell Disease. New England 
Journal of Medicine, 376(16), pp.1561-1573. 
4. Bainbridge R, Higgs D, Maude G, Serjeant G. Clinical presentation of 
homozygous sickle cell disease. The Journal of Pediatrics. 1985;106(6):881-
885. 
5. Gladwin M, Vichinsky E. Pulmonary Complications of Sickle Cell Disease. 
New England Journal of Medicine. 2008;359(21):2254-2265. 
6. Prengler M, Pavlakis S, Prohovnik I, Adams R. Sickle cell disease: The 
neurological complications. Annals of Neurology. 2002;51(5):543-552. 
 
 
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Sickle Cell Disease

Vyas, Rahul

Prasad, Rajendra

Digital Journal of Clinical Medicine 
Volume 1 Issue 1 Article 5 
2019 
HIV with Opportunistic Neuroinfection 
Rahul Vyas 
JSS AHER 
Rajendra Prasad 
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 
Vyas, Rahul and Prasad, Rajendra (2019) "HIV with Opportunistic Neuroinfection," Digital Journal of 
Clinical Medicine: Vol. 1: Iss. 1, Article 5. 
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. 
HIV with Opportunistic Neuroinfection 
Rahul Vyas, 7th term MBBS, JSS Medical College, JSS AHER 
Dr. Rajendra Prasad, Associate Professor, General Medicine, JSS Medical College, JSS 
AHER 
 
CLINICAL HISTORY: 
34 year old male with complaints of:  
-Fever since 2 days, moderate grade, associated with chills and rigors 
-Unresponsiveness since 2 days 
Known case of HIV since one year, non-adherent to Anti-retroviral therapy medication 
Known case of Miliary TB was treated with Anti-Tubercular therapy (ATT) 1 year back.  
Known case of Seizure disorder on medication  
(Tab. Levetiracetam) 
 
EXAMINATION AND INVESTIGATIONS: 
CNS Examination: 
-Patient was conscious, not oriented, was not obeying oral commands 
-Neck Rigidity was present 
-Kernig sign was positive 
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• Bilateral pupils are equal and reactive 
• Cerebellar Signs – Not Elicited 
CVS: S1 S2 heard. No Murmurs 
Respiratory System: Bilateral normal vesicular breath sounds heard. No adventitious sounds 
Per Abdomen: Soft, Non-tender, No organomegaly. Bowel sounds heard. 
Fundoscopy: Normal 
CSF Analysis:  
Cell count: 42  
98% Lymphocytes, 
2% Neutrophils 
CSF LDH: 223 U/L 
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ZN Staining:  
Negative for AFB 
Cryptococcal Capsular Polysaccharide Antigen: Positive in Serum and CSF 
CD4 count: 63cells/mm3 
HIV Viral Load: 36936 copies/mL  
Sodium: 121mEq/L 
Potassium – 3.5mEq/L 
Chloride – 85mEq/L 
USG Abdomen and pelvis: Bulky Kidneys and Splenomegaly.  
CT Brain: Bilateral ill-defined hypo-densities in the frontal, insular and temporal lobes 
suggestive of Progressive Multifocal Leukoencephalopathy (PML)  
 
                  
 
FINAL DIAGNOSIS: 
• HIV with  
-TB Meningitis (TBM) 
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-Cryptococcal Meningitis 
-Progressive Multifocal Leukoencephalopathy 
• Hyponatremia probably due to SIADH. 
DISCUSSION:  
HIV positive patients are at an increased risk of opportunistic infections (O.I) like 
Tuberculosis. It can present as Pulmonary and Extra-Pulmonary manifestations.  
Neuroinfections like TBM and Cryptococcal meningitis are common, predisposition to 
certain infection depends on CD4 count. These can give rise to complications with a high 
mortality rate. (1) Starting ART early prevents these complications. Resistance to drugs and 
failure to ART is mostly due to non- adherence to the treatment. It is important to monitor all 
patients regularly for clinical, immunological and virological failure. (2) 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
 
1. Vinnard C, Macgregor RR. Tuberculous meningitis in HIV-infected individuals 
[Internet]. Current HIV/AIDS reports. U.S. National Library of Medicine; 2009. 
Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131531/ 
2. Bezabih YM, Beyene F, Bezabhe WM. Factors associated with first-line antiretroviral 
treatment failure in adult HIV-positive patients: a case-control study from Ethiopia 
[Internet]. BMC infectious diseases. BioMed Central; 2019 [cited 2019Sep20]. 
Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582596/ 
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HIV with Opportunistic Neuroinfection

Gera, Mehak

Babu, Suresh

M, Manthappa

Digital Journal of Clinical Medicine 
Volume 1 Issue 2 Article 8 
1-1-2019 
Cerebro-Vascular Accident 
Mehak Gera 
JSS AHER 
Rajendra Prasad 
JSS AHER 
Suresh Babu 
JSS AHER 
Manthappa 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 
Gera, Mehak; Prasad, Rajendra; Babu, Suresh; and M, Manthappa (2019) "Cerebro-Vascular Accident," 
Digital Journal of Clinical Medicine: Vol. 1: Iss. 2, 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. 
Cerebro-Vascular Accident 
 
Ms Mehak Gera, 5th Term MBBS, Dr.S.Rajendra Prasad, Dr.Suresh Babu, Dr.Manthappa,  
Dr.Varsha T, Department Of General Medicine, JSS Medical College, JSS AHER, Mysuru  
CLINICAL HISTORY: 
63 year old male patient presented with 
Slurring of speech since 1 day associated with deviation of angle of mouth to the left side. 
No history of weakness of limbs, loss of consciousness, seizures, fever, altered sensorium. 
Patient was newly detected to be hypertensive. 
No h/o diabetes mellitus. 
No history of Smoking. 
History of consumption of Alcohol since 10-15 years 
 
EXAMINATION AND INVESTIGATIONS: 
A 63 year old male patient moderately built and nourished, well oriented to time place and 
person. 
No pallor, icterus, 
clubbing, cyanosis, lymphadenopathy, edema. 
VITALS- 
PR:64b/m 
BP:220/110mmHg 
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RR:16 cycles/min 
SpO2:97% on room air. 
SYSTEMIC- 
CVS-S1 S2 heard, no murmurs. 
RS-Bilateral NVBS 
PA-Soft, non-tender 
CNS-Conscious, higher functions intact. 
Patient had UMN facial Palsy in the form of 
Deviation of the angle of the mouth towards the left side. 
Patient able to close the eyes properly and wrinkling of the forehead present bilaterally 
Dysarthria present. 
Other cranial nerves normal. 
Motor- 
Deep tendon reflexes- normal 
Plantar- B/L flexor 
UL- Left side power-5/5, right side-Weakness of the distal muscles of the small muscles of 
the hand 
LL- left side-5/5, right side-5/5 
Sensory- normal 
Cerebellum-normal 
Gait- Normal 
 
BLOOD : Hb– 16.1gm/dl 
Tlc – 9350cells/cumm 
Rbc count – 4.64million/cumm 
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Platelet count – 2lakh/cumm 
Reticulocyte count – 2.6% 
MCV – 98.1fl, MCH – 34.7pg 
MCHC-35.4gm/dl 
Peripheral Blood Smear: Normocytic normochromic blood picture. 
RBS-121mg/dl 
Uric acid-5mg/dl 
LFT- Normal 
Carotid Doppler- 
-Diffuse atherosclerotic disease of bilateral carotid vessel system. 
-Mixed plaque in right carotid bulb causing no significant luminal narrowing/ haemodynamic 
changes. 
Fundoscopy normal. 
ECHO- 
-Concentric left ventricular hypertrophy 
-No regional wall motion abnormality, clots, vegetation, pericardial effusion. 
-normal left ventricular systolic function, EF- 64% 
-Grade I L.V Diastolic dysfunction. 
MRI Brain Report- 
-acute infarcts in left corona radiata and capsuloganglionic region. 
-age related cerebral atrophy with few chronic small vessel ischaemic changes. 
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FINAL DIAGNOSIS: 
Newly detected Hypertension with Facio-brachial monoparesis on Right side 
DISCUSSION:  
Treatment: Tab Atorvastatin 40mg P/O Stat and HS 
Tab Asprin 75mg P/O HS 
Tab Clopidogrel 75mg HS 
Tab Cilnidipine 10mg 1 BD 
Inj. Citicoline 500mg IV 
Inj. Thiamine 500mg IV Q8H 
Speech therapy in view of dysarthria. 
Cerebrovascular accident or stroke is when blood flow to a part of brain is stopped either by a 
blockage or the rupture of blood vessels. It is of two types- an ischemic stroke caused by a 
blockage, a haemorrhagic stroke caused by the rupture of a blood vessel.(1) Both types of 
stroke deprive part of the brain of blood and oxygen. 
Ischemic stroke is the most common. 
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Symptoms of cerebrovascular accident varies depending on the site of the lesion.(2) 
-dysarthria, 
-facial muscle weakness or numbness 
-paralysis of of one side of the body or weak muscles 
-dizziness 
-blurred vision 
-loss of balance and coordination 
-difficulty in walking 
-rapid involuntary eye movement 
Investigation; CT or MRI of the brain 
Treatment of cva- 
Drugs like – 
If the patient comes in the golden hour( within 3 hours), thrombolytic like Tissue 
Plasminogen activator like Alteplase is given. Before using it CT brain to be done to rule out 
Haemorrhage. 
Other medications like antiplatelets, statins(plaque stabilizer),are given. antihypertensive 
drugs if required is given. 
Speech therapy, occupational therapy, physiotherapyare provided depending on the 
deformity. 
Faciobrachial monoparesis is presumed to be secondary to lesions involving Heubner artery 
(a proximal perforating branch from anterior cerebral artery) or lateral lenticulostriate 
artery(branch of middle cerebral artery) Occlusion of these perforating branches causes small 
vessel stroke. Hypertension and age are principal risk factors of these small artery strokes.(3) 
 
ACKNOWLEDGEMENTS:  None  
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REFERENCES:  
1. Andrade SE, Harrold LR, Tjia J, Cutrona SL, Saczynski JS, Dodd KS, Goldberg RJ, 
Gurwitz JH. A systematic review of validated methods for identifying cerebrovascular 
accident or transient ischemic attack using administrative data. 
Pharmacoepidemiology and drug safety. 2012 Jan;21:100-28. 
2. ACLS Suspected Stroke Algorithm [Internet]. [cited 2019 Oct 17]. Available from: 
https://www.acls.net/acls-suspected-stroke-algorithm.htm 
3. Jain SH, Prashanth S, Bhat SS, Jayaraj SG. Faciobrachial Monoparesis secondary to 
borderzone Infarct : A Case Report. J Pub Health Med Res, 2013;1(2):108-09 
 
 
 
 
 
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DOI: –


Cerebro-Vascular Accident

Jain, Riya

KC, Shashidhara

Savitha, Savitha

Digital Journal of Clinical Medicine 
Volume 1 Issue 1 Article 4 
2019 
Sheehan Syndrome 
Riya Jain 
JSS AHER 
Shashidhara KC 
JSS AHER 
Savitha Savitha 
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 
Jain, Riya; KC, Shashidhara; and Savitha, Savitha (2019) "Sheehan Syndrome," Digital Journal of Clinical 
Medicine: Vol. 1: Iss. 1, Article 4. 
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. 
Sheehan Syndrome 
Ms Riya Jain, 2nd year MBBS, Dr. Shashidhara KC, Professor, General Medicine, Dr. 
Savitha, Assistant Professor, General Medicine, JSS Medical College, JSS AHER  
 
CLINICAL HISTORY: 
30 year old year lady, complains -extreme fatigue and myalgia since 2 days. The patient was 
unable to carry out activities of daily living. 
• nausea (not accompanied by vomiting) since 2 days, was predominantly present after 
having her meals. 
• bloating sensation, regurgitation after having her meal and constant abdominal 
discomfort since 2 days. 
Known case of hypothyroidism, on medication. 
(Tab. Thyroxine sodium 100mg BD) 
History of similar incident 
10 days back. She visited the hospital for a check up and was diagnosed with acute 
gastroenteritis. When the symptoms reappeared, she came back to the hospital. Even after 
correction of electrolytes, her sodium levels did not get corrected, suggestive of adrenal 
dysfunction. 
Patient gives past history of excessive per vaginal bleeding post abortion.  
Patient is a mother of three children. The fourth pregnancy was aborted. The abortion was 
followed by excessive vaginal bleeding for a few days. 
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EXAMINATION AND INVESTIGATIONS: 
General Physical Examination: 
• Moderately built and nourished, is alert, cooperative and well oriented. 
• Postural hypotension. 
BP (supine) - 120/90mmHg 
BP (standing) - 102/80mmHg 
-No pallor, no icterus, no clubbing, no cyanosis, no lymphadenopathy, no oedema. 
CVS Examination: 
S1 & S2 heard, No murmurs. 
RS Examination: 
Bilateral normal vesicular breath sounds heard, No adventitious sounds. 
Per Abdomen: 
Soft and non-tender with no organomegaly. 
CNS Examination: 
Conscious and oriented. 
Urine routine examination, Liver Function Test, Serum creatinine and Blood urea: Normal. 
Serum Electrolytes: 
Sodium: 124mEq/L 
Potassium: 4.4mEq/L 
Chloride: 89mEq/L 
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In view of euvolemic hyponatremia and postural hypotension, serum cortisol and serum 
ACTH investigations done. 
Serum cortisol: 1.12ug/dL 
Serum ACTH: not detectable. 
MRI:  
• Mild cerebral atrophy with bilateral discrete white matter hyperintensities 
• Sella turcica is filled with cerebrospinal fluid and the infundibulum is seen traversing 
to the grossly atrophied pituitary gland seen flattened against the floor – Suggestive of 
Empty Sella Turcica. 
  
 
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FINAL DIAGNOSIS: 
• Hypothyroidism 
• Hyponatremia secondary to adrenal insufficiency (Autoimmune polyglandular 
syndrome type II) 
• Empty Sella Turcica syndrome. 
Treatment Given: 
• Tab. Thyroxine sodium 100mg to be continued 
• Cap. Omeprazole and domperidone (once a week) 
• Calcium with vitamin D tablets 500mg OD 
• Tab. Prednisolone 20mg  
• Tab. Fludrocortisone acetate 100mg 
 
 
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DISCUSSION:  
Sheehan syndrome is a state of postpartum hypopituitarism resulting from infarction of the 
pituitary secondary to postpartum hemorrhage or shock and is significant cause of morbidity 
and mortality in less developed countries [1] 
The pituitary gland in pregnancy is more susceptible to ischemia owing to increased pituitary 
volume secondary to hyperplasia of lactotrophs and other cells of the anterior pituitary. 
Following post-partum hemorrhage and severe hypotension, there is partial or complete loss 
of the anterior pituitary hormones, namely the ACTH, FSH, LH, GH prolactin & TSH, 
thereby imparing their target organ functions [2] 
Patients suffering from such pituitary atrophy are likely to present with adrenal insufficiency, 
agalactorrhea, oligomenorrhea and hypothyroidism (Clinically presenting as bradycardia, 
fatigue, hypotension, weight gain, constipation and loss of axillary and pubic hair). [3][4] 
MRI of the pituitary: 
1. Early findings: Enlarged enhancing pituitary 
2. Late findings: Empty Sella 
 
ACKNOWLEDGEMENTS:  None  
 
 
 
 
 
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REFERENCES:  
1. Woodmansee WW. Pituitary Disorders in pregnancy. Neurol Clin. 2019 
Feb;37(1):63-83. [PubMed] 
2. Wang CZ, Guo LL, Han BY, Su X, Guo QH, Mu YM. Pituitary Stalk Interruption 
Syndrome: From Clinical Findings to Pathogenesis. J. Neuroendocrinol. 2017Jan; 
29(1) [PubMed] 
3. Karaca Z, Hacioglu A, Kelestimur F. Neuroendocrine changes after aneurysmal 
subarachnoid haemorrhage. Pituitary. 2019 Jan 2014 [PubMed] 
4. Karaca Z, Laway BA, Dokmetas HS, Atmaca H, Kelestimur F. Sheehan Syndrome. 
Nat Rev Dis Primers. 2016 Dec 22; 2:16092. [PubMed] 
5. Matsuazki S, Endo M, Ueda Y, Mimura K, Kakigano A, Egawa-Takata, et al. A case 
of acute Sheehan’s syndrome and literature review: a rare but life-threatening 
complication of post-partum haemorrhage. BMC Pregnancy and childbirth. 
2017Jun14;17(1): 188. [PubMed]  
 
 
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Sheehan Syndrome

Prabhu, Pratheek

Digital Journal of Clinical Medicine 
Volume 1 Issue 2 Article 7 
1-1-2019 
Ectopia Lentis 
Pratheek Prabhu 
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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 
Prabhu, Pratheek (2019) "Ectopia Lentis," Digital Journal of Clinical Medicine: Vol. 1: 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. 
Ectopia Lentis 
 
 Dr Pratheek Prabhu, JSS Medical College, JSS AHER 
CLINICAL HISTORY: 
52 year old male presented with complaints of decreased vision and glare in both eyes since 
childhood which has worsened over past 6 months 
No h/o pain, redness, watering, photophobia or haloes around light. He has no complaints of 
trauma to eye and no complaints of hearing difficulty. 
Past Ocular History : Evaluated in other centers and was made aware of the disease and was 
using glasses since college days. 
▪ History of using spectacles since 30 yrs:- 
▪ Glasses last changed 6 months back 
▪ Both eyes – +3.00 spherical – 6/18 add +2.50 N-12 
General Medicine and surgical history: 
▪ Marfan’s syndrome with aortic regurgitation 
▪ Oral beta blockers – Toprol XL 50mg BD daily (Metaprolol) 
Family history: 
▪ No known family members with Marfan’s syndrome 
▪ His 21 yr. old son has Marfanoid features 
 
EXAMINATION AND INVESTIGATIONS: 
OCULAR EXAMINATION: 
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1)Visual acuity   OD  OS 
Unaided – Distant                   Near 6/60 N-36 6/60 N-36 
With Aid 6/24 6/18 
With Pinhole Improvement 6/12p Improvement 6/12p 
2)Colour vision Normal Normal 
3)Field of vision Normal Normal 
4)Hirschberg’s Reflex 15 degree on to nasal side (mild exotropia) Central 
5)Pupillary reaction Brisk Brisk 
6)Ocular motility Full in all gazes Full in all gazes 
SLIT LAMP Examination: 
  OD OS 
1)Eye lids and Eye 
lashes 
Normal Normal 
2)Conjunctiva Normal Normal 
3) Cornea Normal Normal 
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4)Anterior Chamber Deep Deep 
5)Iris Iridodonesis Iridodonesis 
6) Pupil 3 mm , Briskly reacting 3 mm , Briskly reacting 
7)Crystalline lens 
Lenticualar opacification and infero-
temporal subluxation seen 
Lenticualar opacification and infero-
temporal subluxation seen 
8) IOP 16 mm Hg 16 mm Hg 
POSTERIOR SEGMENT EXAMINATION :  
  OD OS 
1)Media Clear Clear 
2) Optic disc Normal with C:D- 0.3 Normal with C:D- 0.3 
3) Vascular 
arcades 
Normal Normal 
4)Peripheral retina Normal Normal 
5)Macula 
Foveal reflex present Myopic fundus 
seen 
Foveal reflex present Myopic fundus 
seen 
MUSCULO-SKELETAL EXAMINATION : 
Tall & thin stature 
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Disproportionately long limbs.  
Arm span > height : 190.5 cm > 189.5 cm   
Cardio-vascular system 
Pulse: 76/min. 
BP: 130/80 mmHg 
S1 & S2 – Audible 
Murmur – EDM in left 3rd ICS 
Apex beat – palpable in left 6th ICS 
 
ECG : Tall QRS Complex in leads V4, V5 , V6 
Urine for Sodium Nitroprusside test : Negative 
Urine for Homocysteine level : 6 µmol/g creatine 
Blood for Homocysteine level : 10µmol/L 
RBS : 104 mg/dL 
Hbs Ag (Card method) : Negative 
HIV (Card method) : Negative 
FINAL DIAGNOSIS: 
DIFFERENTIAL DIAGNOSIS : 
Homocystinuria 
Weill-Marchesani syndrome 
Final Diagnosis: ECTOPIA LENTIS DUE TO MARFAN SYNDROME 
 
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DISCUSSION:  
A proper estimation of the refractive error through both the phakic and aphakic portions has 
to be done. 
Check the acceptance in dim light and daylight conditions to yield a better visual outcome 
Await Vitreoretinal Surgeon opinion for Barrage laser before planned cataract surgery 
Planned surgery :- Pars plana lensectomy with anterior vitrectomy and Retro-fixation IOL 
Marfan syndrome (MFS) is a genetic disorder of the connective tissue . MFS is an autosomal 
dominant disorder. About 75% of the time, the condition is inherited from a parent, while 
25% of the time it is a de novo mutation. About 1 in 5,000 to 10,000 individuals have Marfan 
syndrome. It occurs equally in males and females and equally present across different regions 
and different races.4 
Marfan syndrome is caused by mutations in the FBN1 gene on chromosome15 which 
encodes fibrillin-1, a glycoprotein component of the extracellular matrix. Fibrillin-1 is 
essential for the proper formation of the extracellular matrix, including the biogenesis and 
maintenance of elastic fibers.4 
The extracellular matrix is critical for both the structural integrity of connective tissue, but 
also serves as a reservoir for growth factors. Elastic fibers are found throughout the body, but 
are particularly abundant in the aorta, ligaments and the ciliary zonules of the eye; 
consequently, these areas are among the worst affected. 
Diagnostic criteria of MFS were agreed upon internationally in 1996. A diagnosis is based on 
family history and a combination of major and minor indicators of the disorder, rare in the 
general population, that occur in one individual – for example: four skeletal signs with one or 
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more signs in another body system such as ocular and cardiovascular in one individual – 
REVISED GHENT CRITERIA (2010 )4 
Marfan Syndrome can involve skeletal system , eyes , cardiovascualar system , lungs , 
nervous system . 
In eyes usually there is weakness in the ciliary zonules, the connective tissue strands which 
suspend the lens within the eye. The mutations responsible for Marfan syndrome weaken the 
zonules and cause them to stretch. The inferior zonules are most frequently stretched 
resulting in the lens shifting upwards and outwards .1 
Management of Ectopia lentis :- Pars plana lensectomy with anterior vitrectomy and Retro-
fixation IOL1 
There is no cure for Marfan syndrome . Management often includes the use of beta blockers 
such as propranolol or if not tolerated calcium channel blockers or ACE inhibitors4 . If the 
dilation of the aorta progresses to a significant-diameter aneurysm , causes a dissection or a 
rupture, or leads to failure of the aortic or other valve, then surgery (possibly a composite 
aortic valve graft or valve-sparing aortic root replacement) becomes necessary4.However the 
life expectancy has increased significantly over the last few decades and is now similar to 
that of the average person. 
 
ACKNOWLEDGEMENTS:  None  
 
REFERENCES:  
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1. Jack J Kanski , Clinical ophthalmology-A systemic approach 7th edition , 2015;630-
631 
2. AK Khurana , Comprehensive Ophthalmology 6th edition , 2015 ; 215-217 
3. Parsons’ Diseases of the Eye , 22nd edition , 2015;275 
4. Harrison’s Principles of Internal Medicine, 18th Edition , 2012;3212 
 
 
 
 
 
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Ectopia Lentis

Agarwal, Minal

Digital Journal of Clinical Medicine 
Volume 1 Issue 2 Article 10 
1-1-2019 
Immune Thrombocytopenia 
Minal Agarwal 
JSS AHER 
Rajendra Prasad 
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 
Agarwal, Minal and Prasad, Rajendra (2019) "Immune Thrombocytopenia," Digital Journal of Clinical 
Medicine: Vol. 1: Iss. 2, 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. 
Immune Thrombocytopenia 
Ms Minal Agarwal, 5th term MBBS, Dr. S. Rajendra Prasad, Associate Professor, 
Department of General Medicine, JSS Medical College, JSS AHER, Mysuru  
 
CLINICAL HISTORY: 
24 year old lady presented with complaints of:  
1. Increased duration of menstrual flow, associated with passage of clots for 13days. 
2. Bleeding gums lasting for around 5 days associated with bleeding from lips. 
3. Small red brown coloured rashes present all over the body. 
Patient was previously treated elsewhere and was found to have severe anemia and 
thrombocytopenia where she received 3 units of packed red cells (PRBC) and 4 units of 
random donor platelet concentrate (RDP), and was referred to JSS Hospital for further 
management. 
No history of fever 
No history of any allergy. 
No similar complaints in the past. 
No other comorbidities like DM, HTN, Thyroid or Asthma 
No past h/o menstrual irregularities 
 
 
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EXAMINATION AND INVESTIGATIONS: 
General:  
Moderately built and nourished. 
Pallor- Grade 3  
Mucocutaneous bleed present.  
Petechial rash present over left thigh and palate.    
 
Vitals:  
PR : 104bpm  
BP : 130/90mmHg   
RR : 27cycles/min  
SpO2 : 96%    
 
Systemic:    
CVS: S1 S2 heard,        
sinus tachycardia,  
no murmurs.    
RS: Normal.    
PA : Soft.   
No  organomegaly    
CNS: Conscious, oriented.  
 
Blood:  
Hb: 6.4gm/dl  
TLC: 21390cells/cumm  
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RBC count: 2.72million/cumm  
Platelet count: 0.04lakh/cumm  
Reticulocyte count: 3.0%  
MCV: 76.8fl  
MCH: 23.5pg  
MCHC: 30.6gm/dl  
PT: 14.4  
APTT: 23.5    
 
Iron profile:  
Iron: 35.54ug/dl (50-170ug/dl)  
Tibc: 349ug/dl (270-450ug/dl)  
Ferritin: 61.28ng/ml (10-120ng/ml)  
PCV: 25.5% (36-46%)  
Bleeding time: 10 min(2-5 minutes)  
Clotting time: 9 min (3-8 minutes)    
 
Peripheral  Blood Smear:  
Microcytic Hypochromic Anemia with neutrophilic leukocytosis and thrombocytopenia    
 
Others:  
HCV/HIV/HBsAg: Negative  
Dengue NS1: Negative  
Dengue IgM Ab: Negative  
Weil Felix Test: Negative  
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ANA: Negative  
Direct Coombs Test: Negative  
Urine Routine : Normal  
LFT, RFT: Normal  
Thyroid Profile: Normal    
Bone marrow Study: Normocellular marrow with megakaryocytic hyperplasia suggestive of 
peripheral platelet destruction.    
Ultrasound Abdomen and pelvis: Within Normal Limits    
 
At the time of discharge:  
Hb: 7.6gm/dl  
TLC: 12540cells/cumm  
Platelet count: 1.86lakh/cumm  
 
FINAL DIAGNOSIS: 
Idiopathic thrombocytopenic Purpura (ITP) with Severe Anemia 
 
Treatment Given: 
PRBC Transfusion  
Platelet Transfusion  
Tranexamic acid(1gm IV) *6 days  
Dexamethasone(4mg IV) * 2 days Followed by  
Prednisolone(40mg)*5 days  
9Azathioprine(50mg) * 5 days  
Romiplostim(250mcg stat inj)  
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Iron Supplementation    
 
Advice on Discharge:    
Azathioprine (50mg)*30 days (1-0-0)  
Prednisolone(40mg to taper 5mg every 5th day) (1-0-0)  
Protein powder (1-0-1) (2tsp in a glass of milk)  
Iron + Folic acid tab (1-0-0)* 1 month  
Calcium + Vitamin tab (0-1-0)* 1 month      
DISCUSSION:  
Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic 
purpura, is an immune-mediated acquired disease of adults and children characterized by 
transient or persistent decrease of the platelet count and, depending upon the degree of 
thrombocytopenia, increased risk of bleeding.[1]  Petechia, purpura, and easy bruising are 
expected in ITP. Less common are epistaxis, gingival bleeding, and menorrhagia. Uncommon 
findings are gastrointestinal (GI) bleeding, gross hematuria and intracranial hemorrhage.[2]   
 
The diagnosis remains one of exclusion, after other thrombocytopenic disorders are ruled out 
based on history, physical examination, and laboratory evaluation. [3] Diagnosis is by doing 
Bone marrow study Which shows Giant Megakaryocytes with increased number of 
Megakaryocytes[4]    
 
There are many treatment options.  
Initial Treatment Prednisone (7-10 days) or Dexamethasone(4 days every 2 weeks for 4 
cycles) +  IVIG(2 days) or Anti-D +Platelets(if bleeding)  
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Relapsed/Persistent ITP Rituximab(iv weekly for 4wks) or Anti-D or IVIG(iv for 2days) or 
Romiplostim/Eltrombopag    
 
Persistent/Worsening  ITP Azathioprine/danazol or Cyclosporine or chemotherapy. 
Splenectomy  
 
ACKNOWLEDGEMENTS:  None  
REFERENCES:  
1. Cooper N, Bussel J. The pathogenesis of immune thrombocytopaenic purpura. Br J 
Haematol.2006;133:364-374.  
2. Kuwana M, Okazaki Y, Satoh T, Asahi A, Kajihara M, Ikeda Y. Initial laboratory 
findings useful for predicting the diagnosis of idiopathic thrombocytopenic purpura. 
Am J Med. 2005;118:1026–33. 
3. Cines DB, McMillan R. Management of adult idiopathic thrombocytopenic purpura. 
Annu Rev Med. 2005;56:425–42. 
4. Cines DB, Bussel JB. How I treat idiopathic thrombocytopenic purpura (ITP) Blood. 
2005;106:2244–51. 
 
 
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