A nurse is caring for a patient who received an allogeneic hematopoietic stem cell transplant 14 days ago. The patient develops a fever of 101.8°F (38.8°C), has a maculopapular rash on the trunk and extremities, and reports severe diarrhea with 8-10 watery stools per day. Laboratory results show elevated liver enzymes (ALT 180 U/L, AST 165 U/L). What is the nurse's priority intervention?

The patient is at day +14 post allogeneic hematopoietic stem cell transplant (HSCT) and presents with a classic triad: a maculopapular rash on the palms and soles, persistent diarrhea exceeding 500 mL/day, and elevated liver enzymes (ALT 180 U/L, AST 165 U/L). This constellation of symptoms affecting the skin, gastrointestinal tract, and liver is highly specific for acute graft-versus-host disease (aGVHD).

In allogeneic HSCT, donor-derived T lymphocytes recognize recipient tissues as foreign. The pathophysiology involves activation of these donor immune cells against host epithelial barriers, antigen-presenting cells, and effector lymphocytes in target organs. The skin, gut, and liver are the most commonly affected sites, and the appearance of symptoms around the second to third week post-transplant aligns with the typical engraftment and early immune reconstitution period during which aGVHD emerges.

The provided evidence underscores that outcomes after allogeneic HSCT "may be adversely affected by infections and transplant-associated complications, contributing to non-relapse mortality (NRM)" ^[1]. Acute GVHD is a major transplant-associated complication and a leading driver of NRM. The reference also highlights the critical role of epithelial barriers and immune interactions modulated by factors such as vitamin D during the peri-transplant period, noting that "mucosal injury, cholestasis and corticosteroid exposure" are significant clinical concerns ^[2]. This directly reflects the pathophysiology unfolding in this patient: the mucosal injury in the gut is causing severe diarrhea, and the cholestatic pattern of liver injury is manifesting as elevated transaminases.

The priority nursing intervention is to administer prescribed immunosuppressive therapy and monitor for infection. The cornerstone of aGVHD management is prompt escalation of immunosuppression to halt the donor T-cell attack on host tissues. Systemic corticosteroids are typically the first-line therapy. Without rapid immune modulation, aGVHD can progress to severe, steroid-refractory disease with high mortality. The digital surveillance approach discussed in the literature aims to support "earlier detection of complications and thereby help reduce NRM" ^[1], reinforcing the principle that early therapeutic intervention for complications like aGVHD is essential.

However, intensifying immunosuppression carries a profound risk: infection. The same reference notes that infections are a co-contributor to NRM alongside transplant-associated complications ^[1]. The patient is already in a severely immunocompromised state post-transplant, and adding immunosuppressive agents further blunts the ability to fight bacterial, viral, and fungal pathogens. Therefore, the nurse's simultaneous priority is meticulous monitoring for signs of infection, as the therapeutic window for controlling aGVHD is also a period of heightened vulnerability to life-threatening sepsis.

• Option 2 (Increase fluid intake and provide electrolyte replacement therapy): While essential supportive care for the patient's ongoing fluid losses from diarrhea, this intervention addresses a symptom rather than the underlying immunological cause. Without controlling the aGVHD-driven mucosal damage, fluid and electrolyte losses will continue unabated. Supportive care is secondary to definitive immunosuppressive therapy.


• Option 3 (Apply topical corticosteroids to the affected skin areas): Topical therapy may provide symptomatic relief for the rash but is insufficient for managing systemic multi-organ aGVHD involving the gut and liver. The life-threatening aspects of this presentation are the visceral organ involvement, which requires systemic, not local, treatment.


• Option 4 (Implement strict isolation precautions and limit visitor access): Infection prevention is a critical component of care for all post-HSCT patients and becomes even more crucial when immunosuppression is escalated. However, this is a protective measure to prevent a complication of the treatment. The immediate, life-saving priority is to initiate the treatment itself—immunosuppression—to stop the active disease process of aGVHD. Monitoring for infection is the direct nursing corollary to administering that therapy.