Asian Journal of Nursing Education and Research. 10(4): October- December, 2020
521
ISSN 2231-1149 (Print)
2349-2996 (Online) DOI: 10.5958/2349-2996.2020.00113.5
Vol. 10 |Issue-04|
October – December| 2020
Available online at
www.anvpublication.org
Asian Journal of
Nursing Education and Research Home page www.ajner.com
RESEARCH ARTICLE
Acute Graft versus Host Disease Post Allogeneic Stem Cell
Transplantation- A case report
Mrs. Abijah Princy B.1*, Mrs. Amalorpavamari Lucas2, Mrs. Jayakumari J.3 1Reader, College of Nursing, Christian Medical College, Vellore – 632 004, Tamil Nadu India.
2Professor, College of Nursing, Acting HOD, Hemato – Oncology Nursing, Christian Medical College,
Vellore – 632 004, Tamil Nadu India. 3Charge Nurse, Bone Marrow Transplant Unit, Christian Medical College, Vellore – 632 004,
Tamil Nadu India.
*Corresponding Author Email: abijahprincyb@gmail.com
ABSTRACT: Allogeneic Stem cell transplantation remains the standard of care in many of the hematological disorders and
genetic disorders. Despite advances in prevention and management of acute Graft versus Host Disease(aGvHD),
it continues to be a major challenge and most common immunogenic complication post Allogeneic stem cell
transplantation accounting for early transplant related morbidity and non relapse mortality. aGvHD is an immune
triggered process, causing profound immune dysregulation and organ dysfunction. GvHD occurs when immune
cells transplanted from a non-identical donor (graft) into the recipient (host) recognize the host cells as ‘foreign’,
thereby initiating a graft-versus-host reaction. It considerably influences the overall success rate of allogeneic
stem cell transplantation imposing a major impact in the quality of life among transplant survivors. Therefore, it
is crucial to understand the pathophysiology, clinical presentation and management of this acute complication in
order to improve clinical outcomes and to foster wholistic nursing care for patients undergoing allogeneic stem
cell transplantation.
KEYWORDS: aGvHD, Allogeneic stem cell transplantation
INTRODUCTION: The only curative therapy for many of the hematological
disorders as well as immune deficiency disorders, inborn
errors of metabolism, genetic disorders and some of the
solid tumors is allogeneic stem cell transplantation.
Despite advances in HLA typing, GvHD intensive
prophylaxis and post transplant immunosuppressive
therapy, GvHD remains a major complication of concern
attributing to transplant related mortality.
Received on 29.06.2020 Modified on 08.08.2020
Accepted on 07.09.2020 ©A&V Publications All right reserved
Asian J. Nursing Education and Research. 2020; 10(4):521-528. DOI: 10.5958/2349-2996.2020.00113.5
aGvHD occurs when the transplanted donor T
lymphocytes recognize antigenic disparities between the
host and recipient. Inflammatory cytokine release has
been implicated as the primary mediator of aGvHD and
activation of T cells is one step in the complex process.
Deregulated cytokine release by cells other than T cells
leads to tissue damage associated with aGvHD.1 aGvHD
predisposes to multi-organ syndromes of tissue
inflammation and or fibrosis that primarily affect skin,
gastrointestinal tract, liver and mucosal surfaces.
Clinically, GvHD is described as acute GvHD when it
occurs within 100 days after Hematopoietic Stem Cell
Transplantation (HSCT) or chronic GvHD which occurs
after 100 days, but these syndromes may overlap in time.
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522
Epidemiology:
Acute GvHD is the second leading cause of death, after
disease relapse following allogeneic HSCT.2 The exact
incidence of aGvHD after allogeneic HSCT is unknown.
Reported incidence rates range from 9 to 50% in patients
who undergo allogeneic HSCT from a genotypically
HLA identical sibling. Acute GvHD is also common in
matched unrelated donors and in haplo identical related
donors.3 With matched related and unrelated donors, the
cumulative incidence of acute GvHD remains
approximately 40-60% respectively.4 It has been
estimated that 20-50% of all transplanted patients
experience grade 2 or more aGvHD despite immuno-
suppressive prophylaxis.1
Risk factors:
The risk factors of aGvHD are multifactorial and have
been studied intensively over the last three decades.
These include:
• Human leukocyte antigen (HLA) disparity
• Increased age in donor and recipient
• Multiparous female donor
• Donor and recipient sex mismatch
• Increased dose of total-body irradiation(TBI)
• Full intensity conditioning regimen
• Ineffective acute GvHD prophylaxis
• Source of the graft/unrelated donor
• Lack of protective environments
• Splenectomy
• Immunoglobulin use
• Pre transplant comorbidities
• ABO compatibility
• Prior exposure to Herpes viruses
• Donor transfusions
• Performance score
• Antibiotic gut decontamination
• Post-transplant transfusion
Further, acute GvHD also differs by disease, Acute
leukemia compared with other hematologic malignancies
is a significant risk factor for aGvHD.5,3 Certain cellular
markers in donor grafts, most notably, the T cell subsets
expressing IL-7 receptor-α (CD127) and PD-1 and
elevated levels of tumor necrosis factor-α in both graft
and patient before HSCT posed risk of aGvHD
development.6 Transplantation with an identical sibling
donor and the use of ATG in the conditioning regimen
containing TBI have been associated with a decreased
risk of grades II–IV aGvHD.7
Classification:
GvHD is sub classified based on the timing of
presentation and the features present as follows:
• Classic acute GvHD: Cases present within 100 days
of HSCT and display features of aGvHD. Diagnostic
and distinctive features of chronic GVHD are absent.
• Persistent, recurrent, late onset acute GvHD:
Cases present greater than 100 days post-HSCT with
features of aGvHD. Diagnostic and distinctive
features of chronic GvHD are absent
• Classic chronic GvHD: Cases may present at any
time post-HCT. Diagnostic and distinctive features of
chronic GvHD are present. There are no features of
acute GvHD.
• Overlap syndrome: Cases may present at any time
post-HSCT with features of both chronic GvHD and
acute GvHD. On occasion, this is colloquially
referred to as "acute on chronic" GvHD.8
Pathophysiology:
GvHD occurs as the donor cells are not identical with the
recipient (patient) cells. This leads to a fight between the
T cells of the donor and the host immune system.
Development aGvHD involves 3 phases as shown below
(Fig 1). Donor T lymphocytes play the crucial role of
mediating GvHD following interactions with activated
host and donor antigen-presenting cells (APC). A
complex network of cytokines, chemokines, cellular
receptors and immune cell subsets then modulate T-
cell/APC interactions that result in GvHD.9 The
inflammatory cascade and continued tissue damage can
lead to release of biomarkers of aGvHD into the
circulation even before the onset of clinical signs of
GvHD potentially predicting therapy responses. These
biomarkers include soluble CD30 from activated T cells,
elafin (skin-specific), regenerating islet-derived 3-α
(REG3α;gut-specific), suppressor of tumorigenicity 2
(ST2; a member of the IL-1 receptor family–binding IL-
33), microRNA and others.10 As counterparts to the
effector cells, the T regulatory cells (T reg) suppress
GvHD and also impairs the target tissue homing of
effector cells.1
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523
Fig 1: Three phase development of aGvHD1
Staging and Grading:
Acute GvHD is clinically graded and staged in severity from grades I to IV depending on the extent of skin, liver
and gut involvement.
Table 1: Sages of aGvHD2
Clinical
stage
Lower GI Upper GI Liver
(Bilirubin level in mg/dl)
Skin
(% rash of body surface area)
1. Diarrhea <500 ml/day Nausea/vomiting 2-3 <25%
2. Diarrhea 500-1000 ml/day 3-6 25-50%
3. Diarrhea 1000-1500 ml/day 6-15 >50% Generalized erythroderma
4. Diarrhea >1500ml/day >15 Bullae/ desquamation
Table 2: Grading of aGvHD2
Overall clinical
grade
Lower GI Upper GI Liver Skin
I 0 0 0 1-2
II 1 1 1 3
III 2-3 2-4 –
IV 4 – 4
Clinical manifestations:
Clinical manifestations of aGvHD include specific
derangements in the skin, liver and gastrointestinal tract,
occasionally the eyes and oral mucosa. It often presents
with skin rash, diarrhea, elevated bilirubin, and it is
associated with recurrent infections.
Acute Skin GvHD:
Characterised by maculopapular rash, sometimes pruritic
or painful. Typically distributed on the palm of the hands
and soles of the feet, later progresses to the face, neck,
upper chest and trunk. Stage III shows generalized
erythroderma with bullae formation and desquamation of
the epidermal layers of the skin.
Acute liver GvHD:
Characterized by an isolated hyperbilirubinemia. The
increase in alkaline phosphatase is seen more frequently
than liver enzyme abnormalities.
Acute Gastrointestinal GvHD:
Exhibit profuse diarrhea with anorexia and sometimes
nausea. Progression with abdominal pain, GI bleeding
and ileus is associated with later stages of GvHD1
The most common target organ of aGvHD is the skin,
followed by the gastrointestinal tract.7 The mortality risk
varies depending on the stage and grade of aGvHD2
Diagnosis:
Diagnosis of aGvHD can be made as follows:
• Clinically in patients presenting with a rash, diarrhea
and elevation of bilirubin within the first several
weeks of transplant.
• Skin and liver biopsies
• Plasma biomarkers: IL-2-receptor-a, TNF receptor-1,
IL-8 and hepatocyte growth factor has been
suggested as a confirmatory tool for the diagnosis of
aGvHD at the onset of clinical symptoms and to
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524
provide prognostic information independent of
GvHD severity.2
Management:
Treatment should be tailored based on the severity of
presentation and symptom management. Calcineurin
inhibitors are the cornerstone of prophylaxis, while
steroids remain the gold standard of treatment.4
• Methyl Prednisolone (Systemic corticosteroid) is
given at 2mg/kg/day given in 2 divided doses in
grade III-IV, while 0.5 to 1mg/kg/day for grade II
disease.
• The original immune suppressive prophylaxis must
be continued. Median time to resolution of aGvHD is
30-42 days.
• In patients who respond to initial therapy, short-term
tapering treatment with prednisone to a cumulative
dose of 2,000mg/m2 is effective and expected to
minimize steroid-related complications.
• In steroid refractory cases, alternative therapies
include antithymocyte globulin (ATG), cyclosporine,
mycophenolate mofetil, anti-IL-2 receptor, anti-CD5-
specific immunotoxin, pan T-cell ricin A-chain
immunotoxin, ABX-CBL, etarnercept, infliximab,
daclizumab, vilizumab and pentostatin. These agents
can be used alone or in combination.
• The use of mesenchymal stem cell in steroid-
refractory aGvHD is found to be useful for patients
with lower grade aGvHD with only skin
involvement. Extracorporeal photopheresis also
shows promise as a less immunosuppressive strategy
to reduce rates of aGvHD.2
Prevention:
Prevention of aGvHD is the most vital dimension in
patients undergoing allogeneic HSCT. Prophylaxis is
mainly based on immunosuppression achieved either by
T cell depletion or pharmacologically. The most
commonly used GvHD prophylaxis following full
intensity conditioning regimen includes a Calceneurin
Inhibitor (e.g. Cyclosporine, Tacrolimus) with
Methotrexate or MMF. Recently, Sirolimus which is a
commonly used immunosuppressant in solid organ
transplantation is also used for GvHD prophylaxis.2
Several studies support that combination of sirolimus
and tacrolimus promoted rapid engraftment, lowered
acute GvHD incidence, reduced transplant-related
toxicity and improved survival.11
Prognosis:
The overall survival at one year is about 20-30%.
Corticosteroid-refractory aGvHD has a poor prognosis
and the second-line therapies have high failure rates.12
• Patients with moderate to severe GvHD have a
significantly higher mortality rate compared with
those with mild disease. Estimated five-year survival
rates of patients with grade III (C) and grade IV (D)
acute GvHD are 25 and 5 percent, respectively.
• Patients with the same grade but different patterns of
skin, gut or liver involvement often have
significantly different outcomes. As an example, a
patient with stage IV cutaneous GvHD alone would
be expected to have a much more favorable outcome
than a patient with stage IV gastrointestinal GvHD
alone, although both have overall grade IV GvHD.13
Nursing Management of a patient with Acute GVHD:
Nursing management in Acute GvHD is discussed using
a case report and nursing process approach
Case Report:
Baby A., a 4 year old is the only daughter of an affluent
non consanguineous parents in Uganda. She was
evaluated in her home town for fever at 1 year of age and
was diagnosed to have Sickle cell Anemia. She also
developed recurrent painful bony crisis and severe back
ache for 3 years with several episodes of upper
respiratory tract infection within 3 months for which she
was repeatedly treated with antibiotics and blood
transfusion. In view of these complaints Baby A. was
referred to a tertiary care hospital in India for definitive
management. On examination, child looked pale, had
hepatomegaly of 2 cm below the right costal margin.
Had no icterus, cyanosis, clubbing, peripheral
lymphadenopathy or splenomegaly. Her mutation
analysis confirmed Homozygous Sickle cell Anemia,
Hemoglobin was 8.9g%, Liver function tests were
elevated (Blirubin-2.47mg/dl, SGOT-62U/L), Serum
Ferritin was 439ng. Ultrasonography of abdomen
revealed small ringed spleen. MRI brain suggested subtle
focal changes of right terminal Internal Carotid artery.
Cardiac, dental and ENT clearance was obtained as part
of transplant work up. Due to unavailability of sibling
donor and matched unrelated donor, Baby A. underwent
Haplo-identical Allogeneic Stem Cell Transplantation
with her mother being the donor (32 years).
HLA typing: HLA: 5/10 A locus B Locus C Locus DR Locus
DRBI
DQ Locus
DQB1
Baby A.
PATIENT
36:01
68:02:01G
15:10:01
58:01:01G
03:04:02
03:02:01G
03:01:01G
07:01:01G
02:01:01G
02:01:01G
Mrs. M
DONOR
02:01:01G
36:01
15:10:01
42:01:01
03:04:02
17:01:01G
03:02:01
03:01:01G
02:01:01G
04:02:01G
Asian Journal of Nursing Education and Research. 10(4): October- December, 2020
525
Conditioning regimen protocol: she received the
following condition regimen and tolerated them without
any complications:
• Inj. Thiotepa 8mg/kg on day -6 (155mg)
• Inj. Treosulfan 14gm/m2/day on day -5, -4 (10gm) to
day -3 (13gm)
• Inj. Fludarabine 40mg/m2/day from day -5, -4, -3 (30
mg) to day-2 (33mg)
• Inj. Rituximab 375mg/m2 (300mg) on day-1
• Total Body Irradiation (200cGy) on day -1
After alpha beta T cell depletion, 190ml of Stem cell
product with CD 34 cell dose of 10.2 x106 cells/Kg was
infused. No immediate complication was noted during
the infusion. She achieved complete chimerism status on
Day 28. Post HSCT, she developed Febrile Neutropenia
from day +12 and multiple infections (Day+33:
Enterococcus faecium and Klebsiella Pneumonia CRO
Sepsis). She received Inj. Amikacin 340mg od, Inj.
Meropenem 750mg Q8h, Inj. Colistin 2.5 MU Q8h, Inj.
Teicoplanin 200mg Q12h, Inj. Metronidazole 150mg and
was on Ionotropic support. For fungal pneumonia she
was managed with Inj. Amphotericin B 50mg od and
Inj.Caspofungin 35mg bd. On day +4, she developed
Grade II mucositis which was managed with Total
Parenteral Nutrition and opioid analgesics infusion.
Mucositis improved as the Neutrophil Engraftment
occurred. Child also developed BK virus and Adeno
virus infection inspite of the prophylaxis with Tab.
Leflunamide 100mg and Inj. Ciprofloxacin 100mg bd.
Hence, she received Inj. Cidofovir 75mg (once a week).
She developed severe painful oral ulcers on day +48 due
to Herpes simplex virus 1 and was given Inj. Acyclovir
10mg/kg for 16 days.
In addition to the T cell depleted stem cell infusion, Inj.
Cyclosporine 480mg bd was given additionally to
prevent GvHD. Child started showing symptoms of
acute Gastro intestinal GvHD since day +12 with
progressively worsening symptoms from grade II to
grade IV disease presenting with diarrhoea, abdominal
distention, pain, paralytic ileus, and hematochezia. She
was initially managed with Inj. Methyl prednisalone
18mg IV and Inj. Octreotide 100mcg od. On day +41
and day +65, she received 2 doses of CD 45 RO cells
(3.7 x106 cell/kg) reinfusion from the cryopreserved
donor samples. She also received IVIG 400mg/kg (10g)
on day +7, +24, +29. Inj. Cyclosporine was stopped as
she developed symptoms of cyclosporine induced
Posterior Reversible Encephalopathy Syndrome (PRES).
She was on low dose of Tacrolimus 0.25mg bd. Inj.
Methyl prednisalone was tapered and stopped as she
developed steroid refractory Gastro intestinal GvHD. Inj.
Ruxolinitib 5mg was given od, Inj. Basiluximab 20mg
IV was given once a week. She was on nil per oral status
on Total Parenteral Nutritional support. On day +100,
she was able tolerate feeds. She got discharged from the
hospital on day +191 during which, she was
asymptomatic, ambulant and on oral diet. She is
followed up in out-patient basis once in 3 months and
subsequently every 6 months. Her day +60 and day +90
chimerism status was complete.
NURSING CARE: 1. Nursing diagnosis:
Actual infection related to immunosuppression
secondary to myeloablative chemotherapy, total body
irradiation, Probable fungal pneumonia, Enterococcus
faecium sepsis, Klebsiella pneumonia CRO sepsis, adeno
virus, BK virus positive status
Expected outcome: Infection is minimised as evidenced
by normothermia, negative blood surveillance culture,
normal chest radiograph, ANC >1500mm3
Nursing interventions
• Inspected for signs of infection including fever,
chills, vomiting, diarrhea, cough. WBC mm3.
Developed fever of 1010 F on day +1 which was
managed with Managed with Inj. Meropenem and
Inj. Amikacin.
• Developed high grade fever, flushing and diarrhoea
on day +11, +16 with signs of septic shock. On day
+33, developed a breakthrough high grade fever,
High resolution CT revealed left lobe superior
segment consolidation. Day +50, blood culture
revealed Enterococcus faecium sensitive to
Teicoplanin, Carbopenemase resistant Klebsiella
pneumonia sensitive to Colistin and Teigicyclin. Inj.
Teicoplanin, Inj. Colistin and Inj. Caspofungin, Inj.
Metronidazole, Inj. Liposomal Amphotericin B,
Ionotropic support
• Monitored the central venous access device site for
infection and performed weekly dressing
meticulously. Hickmann’s catheter was removed on
day +56
• Obtained chest X ray, cultures and sensitivities,
• Regularly monitored (twice a week) for Blood CMV
and urine BK virus reactivation. Started on Tab.
Leflunamide and Inj. Ciprofloxacin (CMV and BK
virus prophylaxis)
• Day +33 developed asymptomatic BK viruria with
quantitative viral load of 10.33 log. Received Inj.
Cidofovir 75mg (once a week). On Day +41
adenovirus PCR became positive. Day +75,
developed high viral load (Log 7.31), restarted Inj.
Cidofovir (4 doses). Developed several painful oral
ulcers at the tongue, floor of mouth and palate. Day
+48: Tissue scraping from oral ulcers revealed HSV
1 Viral PCR was positive (Inj. Acyclovir10mg/kg for
16 days)
• Adopted reverse barrier nursing technique (protective
isolation)
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526
• Ensured vigorous hand washing. Maintained aseptic
technique while performing procedures. Taught on
prevention of infection
• Practiced meticulous oral/ body hygiene
• Instituted low microbial diet with high calories,
proteins, vitamin C, minerals and fluids
• Administered antimicrobial therapy:
Evaluation:
Infection was minimised. Patient had negative blood
culture report. Afebrile. Had clear lung sounds. WBC-
6100/cumm. Day +43, BK virus load became negative.
Tzanck smear was negative.
2. Nursing diagnosis:
Ineffective protection related to Myelosuppression
secondary to chemotherapy/total body irradiation, Gastro
intestinal GvHD, post transplant immunosuppressive
therapy, drug injury (prolonged antimicrobial therapy),
nutritional deficiencies.
Expected outcome:
Patient achieves optimal body functioning as evidenced
by improvement in Gastro intestinal GvHD, general
health status and absence of treatment related
complications.
Nursing interventions:
• Monitored vital signs
• Assessed for post stem cell transplant complications:
• Observed for signs and symptoms of pancytopenia/
myelosuppression. Monitored complete blood counts.
• Administered blood products(Irradiated packed red
cells:20, Irradiated platelet rich concentrates:6, fresh
frozen plasma:7) and granulocyte colony stimulating
factor 50mcg 3/7.
• Monitored for side effects of chemotherapy,
radiation, antimicrobial therapy such as nausea,
vomiting, bone marrow suppression, diarrhoea,
alopecia and infection.
• Assisted in rectal biopsy. Administered steroids and
immunosuppressants.
On day +11 administered Inj. Cyclosporine in addition to
alpha beta T cell depletion of stem cells. On day +12 she
developed Diarrhoea, Rectal biopsy showed Gastro
intestinal GvHD grade 1. Was started on Inj. Methyl
Prednisalone 18mg IV od (+13) to bd (+15). Diarrhea
worsened on day+17(Grade III GvHD). Started on Inj.
Cyclophosphamide 475mg (25mg/kg), Inj. Etanercept
7mg S/C od twice a week, Oral Budesonide
• Assessed the nutritional status. Kept her on nil per
oral status. NG tube to dependent drainage. Provided
parenteral nutrition
• Day +19 she developed cyclosporine induced
Posterior Reversible Encephalopathy Syndrome.
Hence Cyclosporine was stopped.
• Day +23 diarrhoea persisted Inj. Octreotide infusion
was started. Day+30 started on low dose Tacrolimus
(0.25mg bd). Tapered Methyl prednisolone as she
developed steroid refractory Grade IV GvHD.
• Day +45 she developed abdominal distention and
pain suggestive of paralytic ileus.
• Inj. Ruxolinitib (Jakafi) 5mg and Inj. Basiluximab
20mg IV once a week was given as she developed
hematochezia.
Evaluation:
There was marked improvement in GvHD. Infection was
controlled.WBC mm3 Vital signs were stable.
Chimerism was complete on day+28, +60, +90. Was
able to tolerate oral food
3. Nursing diagnosis:
Diarrhoea related to Grade IV Gastro intestinal GvHD,
side effects of conditioning regimen and antibiotic/ drug
intolerance
Expected outcome:
Diarrhoea is controlled as evidenced by patient passing
soft, formed stool not more than thrice a day
Nursing interventions:
• Checked bowel sounds, observed for abdominal
distention, rigidity and pain
• Observed the stool pattern, recorded frequency,
character and volume. Had severe abdominal pain,
loose stools and hematochezia.
• Monitored vital signs for deficient fluid volume
• Obtained stool specimen for culture and sensitivity.
Assisted for rectal biopsy to rule out Gastro intestinal
GvHD grading. Rectal biopsy revealed evidence of
grade IV Gastro intestinal GvHD
• Administered Oral Rehydration Solution after each
episode of loose stools
• Administered IV fluids. Monitored intake output
chart.
• Administered parenteral nutrition, steroids and
antibiotics for GvHD management
Evaluation:
Patient passed soft formed stool. There was complete
improvement in Gastro intestinal GvHD. On day +100
child was able to tolerate oral feeds.
4. Nursing diagnosis:
Impaired oral mucosal membrane related to side effects
of chemotherapy/ total body irradiation
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527
Expected outcome:
She achieves optimal integrity of the oral mucosal
membrane as evidenced by absence of mucositis
Nursing interventions:
• Assessed the oral mucous membrane. Had painful
oral ulcers (Grade II oral mucositis)
• Kept on NPO status, administered Total Parenteral
Nutrition
• Administered opioid analgesics
• Encouraged mouth wash using diluted 7% Sodium
bicarbonate followed by 2% Chlorhexidine solution 4
times/day as the mucositis improved
• Encouraged GvHD diet once tolerant to oral diet
• Encouraged 2-3 litres of water/day
Evaluation:
Grade 2 oral mucositis completely resolved as the
neutrophil engraftment occurred. She was able to tolerate
normal diet.
5. Nursing diagnosis:
Imbalanced nutrition less than body requirement related
to grade IV Gastro intestinal GvHD, side effects of
conditioning regimen, malabsorption of nutrients,
increased metabolic rate secondary to fever/infection
Expected outcome:
Patient achieves optimal nutritional status and protein
stores as evidenced by adequate calorie intake based on
body requirement and weight gain
Nursing interventions:
• Determined specific causes for imbalanced nutrition.
Auscultated for bowel sounds. Assessed the
nutritional status
• Monitored lab values: Hb- 8.9g%, WBC-
6100/cumm, serum Ferritin-439 ng%, total protein-
6.9g/dl, albumin-4.3g/dl
• Evaluated the effectiveness of antiemetic and
antidiarrheal therapy
• Assessed her food preferences
• Administered parenteral nutrition and intravenous
fluids
• Implemented GvHD diet after maintaining NPO
status
• Implemented meticulous oral hygiene with 2%
chlorhexidine solution Q4 hourly
Evaluation:
Child’s nutritional status gradually improved. Parenteral
nutrition was stopped. Paralytic ileus symptoms
resolved. She was able to tolerate oral feeds from day
+100. There was significant weight gain.
6. Nursing diagnosis:
Fatigue related to decreased oxygen carrying capacity of
blood, NPO status, pain, side effects of chemotherapy/
radiation, hyperthermia, infection
Expected outcome:
Child attains optimal energy and activity tolerance as
evidenced by ability to play and perform her ADLs
Nursing interventions:
• Assessed the level of fatigue and the specific causes
of fatigue
• Assisted in planning the ADLs, prioritized the
activities with the parents
• Encouraged frequent rest periods after activity
• Transfused blood when haemoglobin was less than
8g%. She received 20 units of Irradiated Packed red
cells during the peri transplant period
• Encouraged high protein, high calorie diet.
Administered total parenteral nutrition
• Instituted supplemental oxygen therapy(2- 4litres)
• Administered antipyretics(Inj. Febrinil 250mg prn)
and antibiotics/ antifungal and antiviral medications
Evaluation:
There was improvement in child’s energy level. She was
able to perform ADLs and play actively.
7. Nursing diagnosis:
Anxiety (Parental) related to high risk procedure,
uncertainty of treatment outcome and hospitalization
Expected outcome:
Anxiety is minimised as evidenced by adopting positive
coping mechanisms and restful appearance
Nursing interventions:
• Acknowledged awareness of the parent’s anxiety.
Examined anxiety provoking situations
• Reassured and provided a non-threatening
environment
• Oriented them to new experiences, procedures and
people in the Bone marrow transplant Unit
• Involved patient in play therapy
• Encouraged verbalization of feelings and cleared
their doubts in simple language
Evaluation:
Anxiety was minimised. Parents were restful and calm.
They verbalised familiarity over the environment and
procedure
8. Nursing diagnosis:
Knowledge deficit regarding disease process, procedures
and treatments in hematopoietic stem cell
Asian Journal of Nursing Education and Research. 10(4): October- December, 2020
528
transplantation, complications, home care and follow up
related to lack of information
Expected outcome:
Learning needs are met regarding disease process,
procedures and treatments in hematopoietic stem cell
transplantation, complications, home care and follow up
as evidenced by verbalization of understanding by
parents
Nursing interventions:
• Assessed the parent’s level of knowledge and
understanding of disease process, procedures,
treatment plan and follow up after discharge
• Explained on Sickle cell anemia, haplo-identical
allogeneic stem cell transplantation including harvest
procedure, conditioning, engraftment, side effects,
complications including GvHD and the physical set
up of bone marrow transplantation unit
• Explained the need for infection control, care of
central venous access device, antiobiotic/ antifungal/
antiviral therapy, low microbial diet, total parenteral
nutrition and blood transfusion.
• Discussed on follow up schedule and home care
Evaluation:
Parents verbalised understanding and confidence in
caring for Baby A.
CONCLUSION: aGvHD highlights the need for appropriate risk
reduction while HSCT planning, patient tailored
prophylaxis, prompt assessment and monitoring, early
detection aid to appropriate management and expected
treatment outcome. There is a tremendous role of
hematology nurse while caring for patients with aGvHD.
CONFLICT OF INTEREST: The authors have declared no conflicts of interest.
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