Asian Journal of Nursing Education and Research. 10(4): October- December, 2020


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

Asian Journal of

Nursing Education and Research Home page


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:

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.

Asian Journal of Nursing Education and Research. 10(4): October- December, 2020



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


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


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

Asian Journal of Nursing Education and Research. 10(4): October- December, 2020


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



Lower GI Upper GI Liver

(Bilirubin level in mg/dl)


(% 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


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 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

Asian Journal of Nursing Education and Research. 10(4): October- December, 2020


provide prognostic information independent of

GvHD severity.2


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


• 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 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


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


DQ Locus


Baby A.












Mrs. M












Asian Journal of Nursing Education and Research. 10(4): October- December, 2020


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


Asian Journal of Nursing Education and Research. 10(4): October- December, 2020


• 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:


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


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


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



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


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


• Administered parenteral nutrition, steroids and

antibiotics for GvHD management


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

Asian Journal of Nursing Education and Research. 10(4): October- December, 2020


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


• 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


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


• Implemented GvHD diet after maintaining NPO


• Implemented meticulous oral hygiene with 2%

chlorhexidine solution Q4 hourly


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


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


• 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


Anxiety was minimised. Parents were restful and calm.

They verbalised familiarity over the environment and


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


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


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


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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