A
TROJAN
HORSE
Mr. Awadh Kishore Prasad, 63 year elderly male from Ranchi presented (21/02/2024) with
complaints of :
• Maculopapular rash since 7 days
• Fever since 5 days
• Dysphagia since 4 days
Mr. Awadh Kishore was apparently well 7 days back when he developed a maculopapular
rash on the trunk followed by facial puffiness and erythema all over the body .The rash was
initially restricted to the trunk but later involved his abdomen and bilateral lower and upper
limbs over the next 7 days .The rash was associated with itching.
Three days later, he developed high-grade fever with chills, along with dysphagia which
was preceded by oral ulcers and throat pain.
There was no history of dysuria, abdominal pain, breathlessness, cough or bleeding
manifestation. The patient was immediately admitted at a local hospital and found to be
bicytopenic and hence referred to CMC for further management.
Past history
He had a history of Coronary artery disease - POST PCI TO LAD and Stent Placement in
2015 ,was on antiplatelet and atorvastatin.
Hypothyroidism on 75 mcg of eltroxin
He had a history of admission on 21st January- 2024 for hyponatremia, pneumonia
and urosepsis ([Link]) with septic shock for which he was treated with iv antibiotics and
was discharged on 31st January 2024.
He also had a h/o blood transfusion in January in view of anemia during his hospital stay.
Treatment History
During the first admission (January ) he had received meropenem and was discharged on
oral Cefuroxime. While during his second admission (February) he was managed with
Ryles tube due to dysphagia and was empirically started on antibiotics (Inj Ceftazidime
Avibactam, Teicoplanin and Caspofungin ) for febrile neutropenia.
Drug History
Silodosin 21/1/4- 19/2/24
Glimepiride 21/1/4- 20/2/24
Esomeprazole 21/1/24- 7/2/24
Levosulpiride (Antipsychotic medication) 21/1/24- 7/2/24
Acebrophylline 21/1/24 - 7/2/24
Remac (Vitamin b12) - 31/2/24- 7/2/24
Inj. Meropenem 21/1/24- 31/1/24
Tab Cefuroxime 1/02/2024 -7/02/2024
Inj Ceftazidime Avibactam, Teicoplanin and Caspofungin 17/2/24- 20/2/24
Personal history
No addictions
Takes mixed diet
Bowel habits - Normal
Sleep and appetite was normal in the past
Family History
Married and had 2 sons
?
History Diagnosis
Viral Exanthem
Drug Rash
Rickettsia Infection
Examination
Pulse rate : 129/ min
Blood pressure : 111/63 mm Hg
Respiratory rate : 38/ min
SpO2 : 95%
Temperature : 101.5 F
GCS 15/15
Pallor + Icterus +
There were multiple blanching erythematous
maculopapular as well as few purpuric lesions
over the trunk, arms, legs. There was edema and erythema noted over the face with
desquamation over the ear lobes. Palms and soles - There was erythema over the
palms and desquamation over the soles.
Oral mucosa - Yellowish crusting noted over the lips, tongue, buccal mucosa.
Genitialia - Partially able to retract the foreskin which was firm and had minimal
whitish precipitate.
P/A :Soft, non tender, No hepatosplenomegaly
RS :Bilateral wheeze + with crepts all over the chest
CVS :S1 S2 heard and no added sounds
BASELINE PARAMETERS
Biochemistr 22/02/2024
CBC 22/02/2024
y Coagulatio 22/02/2024
Hb 8.6 g /dl Sodium 138 m mol/L n
WBC 100/cumm Parameter
Potassium 3 m mol/l
s
Platelet 103000/ Creatinine 0.68 mg%
PT 20.6 sec
cumm Total/Direct 7.27/6.82
Bilirubin Corrected PT 14.7 sec
MCV 82.4 Fl
Total Proteins 5.2 g/dl APTT 50.6 sec
Retic 0.13
Albumin 2.8 g/dl Corrected 33.3 sec
LDH 372 U/L APTT
SGOT /SGPT 22/89 U/L
INR 1.55
ALP 233 U/L
Fibrinogen 553
Parameters
ANA Negative
Triglyceride 115 mg %
Ferritin 1184 ng/ml
CBC Parameters 20/01/24 24/01/24 27/01/2024 30/01/2024 10/02/2024 17/02/2024 21/02/2024
Hb 12.5 7.9 10.6 10.4 10.6 9.1 8.6
WBC 5600 19200 6300 4400 3700 600 100
WBC Differentials 62/27/3/0/8 89/8/0/0/3 80/10/4/6 77/15/2/0/6 65/25/2/0/8 2/98/0/0/0
(N/L/E/B/M)
Platelets 150000 120000 120000 110000 250000 220000 103000
Septic Screen Virology
Screen
Procalcitonin 1.61 ng/ml BBVS Negative
Leptospira Negative Dengue Negative
(Elisa)
Widal Negative EBV PCR Negative
Weil Felix Negative CMV PCR Negative
Spotted fever Negative Hepatitis Negative
IgM Screen
Peripheral smear Anisocytosis, hypochromic, ovalocytes, target cells and
fragmented rbcs present
Bone marrow aspiration Scanty markedly hypocellular marrow with marked decrease in
hematopoietic cells and increase in RE cells.
Bone marrow Biopsy Markedly hypocellular marrow (overall cellularity ~30%) with
markedly suppressed trilineage haematopoiesis and evidence
of erythrophagocytosis.
BLOOD
CULTURE REPORT
CBC PROFILE
BIOCHEMICAL PARAMETERS
THE PATIENT HAD RECEIVED HIS SON’S
BLOOD IN THE MONTH OF JANUARY
TRANSFUSIO
N
ASSOSCIATE
D
GVHD
SKIN BIOPSY REPORT
The epidermis shows lamellar hyperkeratosis, follicular plugging, preserved
granular layer, mild regular acanthosis, patchy basal cell vacuolation associated
with occasional scattered basal necrotic keratinocytes. Few necrotic
keratinocytes are also seen in the mid spinous layer. The superficial dermis
shows mild edema, telangiectasia, mild perivascular and mild interstitial
infiltrates of lymphocytes and histiocytes. Yeast forms of fungal organisms are
seen on the
surface. There is no basement membrane prominence.
Patchy interface change with occasional necrotic keratinocyte in the
mid spinous and superficial
dermatophytosis, skin biopsy, left chest.
Note: The histological differentials are Graft versus host disease, Grade
I and drug induced aetiology.
National Health and Safety Network Case definition:
A Clinical syndrome occurring from 2 days to 6 weeks after cessation of
transfusion characterised by characteristic rash: erythematous ,maculopapular
eruption centrally that spreads to extremities and may in sever cases ,progress to
generalised erythroderma and haemorrhagic bullous formation ;diarrhoea; fever;
hepatomegaly; liver dysfunction ;marrow aplasia ;and pancytopenia and
characteristic histological appearance of skin or liver biopsy.
What is Transfusion associated GVHD ?
Transfusion associated GVHD occurs from the engraftment of viable donor leukocytes,
particularly T cells, following a transfusion of cellular products.
Under normal circumstances ,a recipients own immune response can prevent TA GVHD.
If patient is immunosuppressed, or if there is an HLA haploidentical match between the
donor and recipient,
the lymphocytes can proliferate in vivo and attack the host tissue.
If the transfused T lymphocytes are
HLA homozygous for one of the
recipient's haplotypes (even in
immunocompetent recipient) ,the
recipient immune system will
consider these cells as self ,so
these T lymphocytes can
engraft ,proliferate and attack the
host.
Blood Component associated with TA
GVHD
Diagnosis : Clinical
Histopathological Skin finding -
Epidermal mononuclear
infiltrates ,basal membrane
degeneration and bullae formation in
the absence of eosinophils.
Bone marrow : presence of aplastic
anemia or a markedly hypocellular
Any non frozen blood component marrow with a lymphohistiocytc
containing viable lymphocytes can infiltrate. Haemophagocytsosis can
potentially cause TA GVHD.
be present.
Fresh blood (<3 days ) has shown to
have caused TA-GVHD more commonly For confirmation: Chimerism can be
than blood that has been stored for
longer time (<7) days, due to decreased done which will be of donor origin.
INDICATIONS FOR
IRRATDIATION
■ TA GVHD is 90% fatal with no
effective treatment available.
■ The best method for the prevention
of TA GVHD is the irradiation of
cellular products by using either
gamma rays or X rays.
■ As per AABB ,25 Gy should be given
to the central part of the unit ,but
with no component of the unit
receiving less than 15 Gy .
Can TA GVHD be prevented by leukoreduction ????
Leukoreduction involves gross removal of leucocytes. It reduces the risk of
1 Non haemolytic transfusion reaction
2 HLA alloimmunisation
3 Transfusion of leukotropic virus (CMV and EBV)
It is considered as a protective intervention but TA GVHD continues to be reported in
leukocyte depletion/reduction era.
The best filters remove a 3 log reduction (99.9%) of [Link] get to 10,000 WBCS,filters
need to remove a 5 log reduction (99.999%) of [Link] have only 1000 residual WBCS,
a 6 log reduction (99.9999%) filter is needed. At this time no such filter exists in
production.
In conclusion, due to the high mortality associated with TA-
GVHD,
prevention is better than cure.
THANK YOU
