Research Connect

M, Rakshith

Digital Journal of Clinical Medicine 
Volume 1 Issue 2 Article 9 
1-1-2019 
Pulmonary Thromboembolism in a case of Alopecia Areata 
Rakshith 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 
M, Rakshith (2019) "Pulmonary Thromboembolism in a case of Alopecia Areata," Digital Journal of 
Clinical Medicine: Vol. 1: 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. 
Pulmonary Thromboembolism in a case of Alopecia Areata 
Mr Rakshith, 9th Term, JSS Medical College, JSS AHER  
 
CLINICAL HISTORY: 
48 year old female, presented to emergency department with breathlessness of 10 days 
duration. Breathlessness was insidious in onset, aggravated on climbing 10 steps, no relieving 
factors, progressed from grade 1 to grade 3 (NYHA). No history of orthopnoea, chest pain, 
fever, cough.  
Patient informs that she had complaints of calf muscle pain the night before, for which she 
was prescribed NSAID for symptom relief, the night before she was brought to the 
emergency department at JSSH. 
Patient was a known case of Alopecia Areata since 6 months and was on steroid therapy for 
the same. No history of diabetes / hypertension.  
 
EXAMINATION AND INVESTIGATIONS: 
General Examination:  
Cushingoid features was noticed on the face. 
Tachypnoea and tachycardia noted. 
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M: Pulmonary Thromboembolism in a case of Alopecia Areata
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Local examination: 
Tenderness and edema of the left calf muscle. 
SpO2-88% at room air  
Systemic examination:  
Cardiovascular system: S1,S2 heard, sinus tachycardia, no murmurs, no added sounds. 
Respiratory system : B/Ll NVBS heard , no added sounds. 
CNS: Normal. 
CBC, RBS, RFT: Normal. 
 
 
ECG: S1Q3T3 with Sinus Tachycardia 
 
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CT Pulmonary angiogram: Acute pulmonary thromboembolism of bilateral pulmonary 
arteries and segmental branches. 
 
 
 
 
Chest X-ray: Prominent pulmonary bay with Cardiomegaly 
Venous Doppler: Deep vein thrombosis involving the left popliteal vein and superficial 
thrombophlebitis of the left short saphenous vein.  
ANA panel: SS-A(Ro-52) positive. 
 
FINAL DIAGNOSIS: 
Acute pulmonary thromboembolism. 
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M: Pulmonary Thromboembolism in a case of Alopecia Areata
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Deep vein thrombosis of left popliteal and superficial thrombophlebitis of short saphenous 
vein.  
Evolving lupus. 
Cushingoid habitus secondary to steroids. 
Treatment Given: 
Thrombolytic agent TENECTAPLASE 0.5mg/kg iv bolus(40 mg) over 5-10 seconds 
Oral Anti-Coagulant: 
Low molecular weight HEPARIN 40mg OD to prevent recurrence of venous 
thromboembolism. 
Referred to Dept of Rheumatology for evolving lupus 
Referred to Dept of Dermatology for review of steroid usage for alopecia. 
DISCUSSION:  
Deep vein thrombosis(DVT) is a common entity seen in hypercoagulable states like 
autoimmune and connective tissue disorders. It is also seen in among patients on long term 
steroid usage. 
The etiopathogenesis of increased risk of VTE in systemic autoimmune diseases is not 
entirely clear but multiple contributors have been explored, especially in the context of 
systemic inflammation and disordered thrombogenesis.[1] 
Venous thromboembolism (VTE) is major health problem and is sometimes complicated by 
lethal pulmonary embolism (PE). Disturbances of the coagulation and anticoagulation 
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systems are important risk factors for VTE. 
Alopecia areata is an autoimmune disease, in which the inflammation can cause VTE.[2] 
Here SS-A(Ro-52) being positive , suggestive of evolving lupus is a risk factor for VTE. 
This patient was on high dose of steroids which could have contributed to VTE. There is 
evidence that steroids may increase the risk of VTE, notably in patients with Cushing 
syndrome, in which steroid-mediated changes in hemostatic and fibrinolytic factors are 
thought to play a role.[3] 
Incidence of pulmonary embolism is around 0.5–1 case per 1000. It has been estimated that 
70% of proven post mortem cases of pulmonary embolism are not even suspected during the 
course of treatment.[4] 
Patients with Alopecia areata are prone for Venous Thrombo Embolism. Any such patients 
coming with sudden onset of breathlessness, Pulmonary Thrombo Embolism has to be ruled 
out 
ACKNOWLEDGEMENTS:  None  
REFERENCES:  
1. Tamaki H, Khasnis A. Venous thromboembolism in systemic autoimmune diseases: 
A narrative review with emphasis on primary systemic vasculitides. Vascular 
Medicine. 2015 Aug;20(4):369-76. 
2. Zöller B, Li X, Sundquist J, Sundquist K. Autoimmune diseases and venous 
thromboembolism: a review of the literature. American journal of cardiovascular 
disease. 2012;2(3):171. 
3. Lieber BA, Han J, Appelboom G, Taylor BE, Han B, Agarwal N, Connolly Jr ES. 
Association of steroid use with deep venous thrombosis and pulmonary embolism in 
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M: Pulmonary Thromboembolism in a case of Alopecia Areata
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neurosurgical patients: a national database analysis. World neurosurgery. 2016 May 
1;89:126-32. 
4. Laack TA, Goyal DG. Pulmonary embolism: an unsuspected killer. Emergency 
Medicine Clinics. 2004 Nov 1;22(4):961-83. 
 
 
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English

Pulmonary Thromboembolism in a case of Alopecia Areata

Arora, Meghna

Prasad, Rajendra

Digital Journal of Clinical Medicine 
Volume 1 Issue 2 Article 6 
1-1-2019 
Snake Bite 
Meghna Arora 
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 
Arora, Meghna and Prasad, Rajendra (2019) "Snake Bite," Digital Journal of Clinical Medicine: Vol. 1: Iss. 2, 
Article 6. 
This Case Report is brought to you for free and open access by Research Connect. It has been accepted for 
inclusion in Digital Journal of Clinical Medicine by an authorized editor of Research Connect. 
Snake Bite 
 
Ms Meghna Arora, 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: 
28 year old male presented with an alleged history of snake bite. 
Patient was allegedly bitten by a cobra at 9:30pm at his home. He was taken to the local 
hospital, given first aid and referred to a higher centre. Patient then had 2 episodes of 
vomiting. Following which, the patient became drowsy, experienced difficulty in breathing 
and eventually became unresponsive. 
He was brought to the hospital in an unresponsive state and was intubated and ventilated. 
On regaining consciousness, he complained of blurring of vision and blackish discoloration 
of the dorsum of the right hand. 
Past history 
Not a known case of type 2 diabetes mellitus, hypertension, ischemic heart disease, epilepsy. 
Personal history 
Bowel and Bladder – normal and regular 
No h/o alcohol consumption or smoking 
 
EXAMINATION AND INVESTIGATIONS: 
Examination 
Local examination: Swelling on right hand present from fingers to the right wrist joint. Mild 
local rise in temperature noted. Blackish discoloration noted on the dorsum of right hand. 
Bite marks not noted. 
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Arora and Prasad: Snake Bite
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CVS: NAD 
RS: NAD 
Nervous system: Reflexes- B/L plantar mute 
Optic nerve examination: 
Direct light reflex: present with sluggishly reactive pupils 
Indirect light reflex: present 
Accommodation reflex: absent 
Counting of fingers at 30cm: absent 
Fundus- Normal 
 
T2W MRI OF BRAIN WITH ORBIT CUTS 
Impression- Multiple Bilateral symmetrical areas of T2 and FLAIR hyper-intensity in the 
caudate and lentiform nuclei, cortex of frontal, parietal and occipital lobes – findings 
correlate with clinical history of Snake bite induced leuco-encephalopathy 
 
ECHOCARDIOGRAPHY 
Impression- global hypokinesia of Left Ventricle 
Depressed left ventricle systolic function, EF- 40% 
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ECG 
ST-T changes in lead I and avL 
 
Cardiac enzymes 
Trop T 0.266ng/ml (0.0127-0.0249) 
CPK- MB – 7.34ng/ml(0-4.94) 
Chest x ray: 
No Radiological abnormalities detected 
 
ECHO at the time of discharge – No regional wall motion abnormality. EF-60% 
FINAL DIAGNOSIS: 
Snake bite with posterior reversible encephalopathy syndrome, respiratory failure and right 
limb cellulitis with Toxic Myocarditis 
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Arora and Prasad: Snake Bite
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DISCUSSION:  
Treatment- 
1] INJ. ANTI SNAKE VENOM – total 30 vials in 5% dextrose over 1 hour in divided doses 
2] INJ. NEOSTIGMINE – 2.5mg iv for 4 days 
3] INJ. ATROPINE – 0.6mg IV for 4 days 
4] TAB. PIRACETAM – 800mg P/O TID for 5 days 
5] Antibiotics 
Debridement of the wound was done. During the follow up patient vision improved slightly. 
He was able to count the fingers at 30cms. 
Poisoning by venomous snake bite is an acute life-threatening medical emergency. In India 
there are about 216 identifiable species of snakes, out of which 52 are known to be 
poisonous. 
Snake venom may have neurotoxic (eg Cobra venom) or hemotoxic (eg vipers) properties or 
both. 
Cobra venom (neurotoxic) binds to Acetyl choline receptors, preventing the interaction 
between Ach and the receptors on postsynaptic membrane thus resulting in neuromuscular 
blockade. The toxin has a direct action on skeletal, cardiac and smooth muscles, nerves and 
neuromuscular junction causing paralysis, circulatory and respiratory failure, cardiac 
arrhythmias, Heart block and cardiac arrest. 
Other symptoms of neurotoxicity may include loss of memory, vision, and/or intellect, Ptosis, 
uncontrollable obsessive and/or compulsive behaviours, delusions, headache, cognitive and 
behavioural problems and sexual dysfunction. 
Viper venom (hemotoxin) interferes with blood clotting. It exhibits both anticoagulant and 
procoagulant effects on blood clotting mechanism resulting in defibrination syndrome or 
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disseminated intravascular Coagulation. They can cause organ degeneration and generalized 
tissue damage. (1) 
Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological syndrome 
characterized by symptoms like headache, seizures, altered consciousness and visual 
disturbances. 
PRES is seen in association with immunosuppressive therapy after transplantation, eclampsia, 
and acute hypertensive encephalopathy associated with renal disease. Few accounts described 
the occurrence of PRES in victims of animal bites such as scorpions, wasps, and snakes. 
The CT and/or MRI of the brain reveal focal regions of symmetric hemispheric edema 
predominating in the parietal and occipital regions.(2) 
Two hypotheses were suggested to explain the pathogenesis of PRES- hypertension 
exceeding the limits of autoregulation, causing breakthrough brain edema, and hypertension 
leading to cerebral autoregulatory vasoconstriction, ischemia, and consequent brain edema. 
Another theory proposed to explain PRES is the role of endothelial dysfunction. (3) 
The visual disturbance which can vary from blurred vision, homonymous hemianopia to 
cortical blindness. Altered consciousness may vary from mild confusion or agitation to coma. 
Other symptoms include nausea, vomiting and brainstem deficits. Seizures and status 
epilepticus are also common. The treatment of PRES is dependent on the cause. 
Cardiac involvement is an infrequently recognized manifestation of snake bites but it is 
uncommon in elapid bites, only reported to occur in cobra bites. The mechanism of cardiac 
involvement in neurotoxic snake bites is not clear but is likely to be due to one of the myriad 
toxins seen in snake venom, which can cause morphological changes, enzyme alterations, 
ultra structural disturbances and genetic alterations of the myocardial tissue.(4) 
ACKNOWLEDGEMENTS:  None  
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REFERENCES:  
1. Bawaskar HS, Bawaskar PH. Snake bite poisoning. Journal of Mahatma Gandhi 
Institute of Medical Sciences. 2015 Jan 1;20(1):5. 
2. Varalaxmi B, Ram R, Sandeep P, Kumar VS. Posterior reversible encephalopathy 
syndrome in a patient of snake bite. J Postgrad Med. 2014 Jan 1;60(1):89. 
3. Ibrahim A, ElSefi T, Ghanem M, Fayed A, Shaban N. A Horned Viper Bite Victim 
with PRES. Case Rep Neurol Med. 2017 Jan 1;2017:1–6. 
4. Agarwal R, Singh AP, Aggarwal AN. Pulmonary oedema complicating snake bite due 
to Bungarus caeruleus. Singapore Med J. 2007 Aug;48(8):e227-230. 
 
 
 
 
 
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Pulmonary Thromboembolism in a case of Alopecia Areata

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