Acute Promyelocytic Leukaemia Presenting as Bleeding in a Minor Burn Patient: A Case Report

1. Introduction

Thermal injuries are a major global health problem, particularly in low- and middle-income countries like South Africa, and scald burns are a leading cause of burn injuries in the paediatric population [1], resulting in significant morbidity and mortality. Acute burn-induced systemic inflammatory response syndrome is a major physiological response to the burn injury and is characterised by a massive release of pro-inflammatory mediators affecting multiple organ systems. Burn injuries depress the immune function, increasing the risk of infection. Burn-associated coagulopathies result from depletion and impaired synthesis of coagulation factors as well as thrombocytopaenia [2]. Notably, Muganza et al. demonstrated that the degree of platelet decline can predict poor outcomes in severe burns if not acted upon [3]. Thrombocytopaenia in burn patients typically occurs during the early phase and often improves by day five to seven of the injury [4]. When pancytopaenia develops or persists, it is often associated with new-onset sepsis warranting a complete septic work-up; a malignancy is not a condition initially suspected due to its low incidence in the setting of acute burns. Acute promyelocytic leukaemia (APL), a subtype of acute myeloid leukaemia, is a rare but potentially fatal malignancy primarily affecting adults [5]. Patients typically present with signs and symptoms of bone marrow failure, including anaemia, neutropaenia, and thrombocytopaenia. The latter may manifest clinically as a bleeding tendency. On examination, there may be evidence of organ infiltration such as hepatosplenomegaly. There are often no clearly identifiable causes, although prior chemotherapy, radiation, and congenital disorders have been described as associated risk factors [6]. The overlap between burn-related physiological derangements and APL-associated coagulopathy may obscure the diagnosis, particularly in the acute setting where wound sepsis identification and management is prioritised. Anaemia, thrombocytopaenia, and neutropaenia disproportionate to the burn severity warrant further investigations for alternative diagnoses.

2. Detailed Case Description

We present a case of a previously well 12-year-old female without any known co-morbidities, who sustained a minor 4% total body surface area (TBSA) hot water burn on her leg on 12 May 2025. Other than reported flu symptoms a week prior, her clinical examination was normal except for the hot water burn, which was appropriately managed at a local community clinic. She was discharged home on paracetamol and ibuprofen and did not warrant referral to the Burn Unit for admission. She presented to Chris Hani Baragwanath Academic Hospital on 18 May 2025 with a history of seven episodes of haematemesis and two episodes of malaena. She was diagnosed as having upper gastrointestinal bleeding (UGIB) secondary to nonsteroidal anti-inflammatory use.

Her vitals included a sinus tachycardia of 176 bpm with a blood pressure of 105/52 mmHg and a temperature of 37°C. On examination, she was found to be pale, warm to the touch, not jaundiced, with minor cervical lymphadenopathy. Her weight was appropriate for her age with a body mass index of 18.7. The rest of the systemic exam was unremarkable with no evidence of hepato- or splenomegaly. The burn wound on her right lower leg was clean.

Her laboratory workup showed a low haemoglobin of 3.3 g/dL, a raised white cell count of 20.8 x10/L, and a low platelet count of 11 x10⁹/L. She was resuscitated and transfused with four units of red blood cells, three units of fresh frozen plasma, and one and a half units of mega units of platelets (one mega unit contains 4 single unit platelets). Pantoprazole and octreotide infusions were also initiated.

With ibuprofen being the suspected trigger for the gastric bleeding and her haemorrhagic shock, she was booked for an emergent gastroscopy. The findings were evidence of a pangastritis with punctate bleeding. Post-procedure, she was admitted on 19 May 2025 to our Burn Unit intensive care unit, intubated, where she was managed by a multidisciplinary team consisting of paediatric and general surgeons, critical care intensivists, critical care-trained nurses, and allied rehabilitation staff.

However, she continued to bleed post-procedure on the pantoprazole infusion. A thromboelastogram was done for her, which displayed a need for cryoprecipitate and further fresh frozen plasma, as well as further blood transfusions. With her low platelet count (18 x 10⁹/L.), fibrinogen (1.3 g/L), and prolonged PTT (33.2 sec), she was diagnosed with disseminated intravascular coagulation. The precipitant of the disseminated intravascular coagulation was then suspected to be a possible toxic shock syndrome from the burn wound. Blood cultures were done, and she was started on empiric Augmentin and clindamycin. The blood cultures yielded no bacterial growth. Her wound showed no signs of local sepsis and was dressed with paraffin gauze during her stay.

She continued to have ongoing transfusion requirements and displayed clinical deterioration with multi-organ dysfunction on 21 May 2025, including gastrointestinal (UGIB), respiratory (ventilator oxygen requirement exceeding 70%), cardiovascular (shock on maximal vasopressors), renal (anuria), hepatic (deranged liver enzymes), and bone marrow failure (bicytopenia).

On the same day, a decision was made to do a peripheral blood smear. The lab confirmed a diagnosis of acute myeloid leukaemia, and the Haematology Department was consulted. Treatment with All-Trans Retinoic Acid (ATRA) and Daunorubicin was started. Subsequently, a Fluorescence In Situ Hybridisation (FISH) test was also requested.

Renal replacement therapy using continuous veno-venous haemodialysis due to her haemodynamic instability was initiated on 23 May 2025. The patient continued to require ongoing multiple blood transfusions and, despite maximal medical therapy, her multi-organ failure and ischaemic tissue injury progressed until therapy could no longer be escalated. The patient subsequently demised on 25 May 2025.

The blood cultures drawn during her clinical deterioration on 22 and 23 May flagged positive post-mortem on 26 May 2025 with a carbapenem-resistant Enterobacterales, Klebsiella pneumoniae and a Pseudomonas putida requiring Meropenem and Colistin.

Table 1. Ms X’s blood results.

Test + (Normal range)	18 May 2025	19 May 2025	21 May 2025	22 May 2025	23 May 2025	24 May 2025	25 May 2025
White cell count (3.90-10.2 X109 /L)	20.8	22.28	87.88	113.85	52.51	23.71	4.69
Haemoglobin (10.3-15.5 g/dL)	3.3	6.4	5.4	7.0	8.1	5.3	5.4
Platelet count (180-440 X109 /L)	11	18	16	28	13	4	5
C-Reactive Protein (<10 mg/L)		245	361		14	300	198
Procalcitonin (<0.1 ug/L)		128	253.20		254	221.2	111.60
Peripheral blood smear			Features in keeping with AML with concern for APL				Features in keeping with known diagnosis .Severe neutropenia
Blood culture		No growth after 5 days	No growth after 5 days	CRE Klebsiella Pneumonia	1.Klebsiella Pneumonia 2.Multi-drug resistant Pseudomona Putida
Urea (1.8-5.7 mmol/L)	11.6	15.6		29.9	36.4	39.9	26.5
Creatinine (37-63 mmol/L)	237	331		625	649	568	314
International Normalized Ratio (<1.1)	1.66	1.57	1.64	1.46		1.59
D-Dimer (<0.25 mg/L)				>17.60	>17.60	>17.60
Flourescence In Situ Hybridization			60% cells positive for translocation t(15;17) q(24;21) . PML/RARA fusion gene

Table 1. Ms X’s blood results.

Test + (Normal range)	18 May 2025	19 May 2025	21 May 2025	22 May 2025	23 May 2025	24 May 2025	25 May 2025
White cell count (3.90-10.2 X109 /L)	20.8	22.28	87.88	113.85	52.51	23.71	4.69
Haemoglobin (10.3-15.5 g/dL)	3.3	6.4	5.4	7.0	8.1	5.3	5.4
Platelet count (180-440 X109 /L)	11	18	16	28	13	4	5
C-Reactive Protein (<10 mg/L)		245	361		14	300	198
Procalcitonin (<0.1 ug/L)		128	253.20		254	221.2	111.60
Peripheral blood smear			Features in keeping with AML with concern for APL				Features in keeping with known diagnosis .Severe neutropenia
Blood culture		No growth after 5 days	No growth after 5 days	CRE Klebsiella Pneumonia	1.Klebsiella Pneumonia 2.Multi-drug resistant Pseudomona Putida
Urea (1.8-5.7 mmol/L)	11.6	15.6		29.9	36.4	39.9	26.5
Creatinine (37-63 mmol/L)	237	331		625	649	568	314
International Normalized Ratio (<1.1)	1.66	1.57	1.64	1.46		1.59
D-Dimer (<0.25 mg/L)				>17.60	>17.60	>17.60
Flourescence In Situ Hybridization			60% cells positive for translocation t(15;17) q(24;21) . PML/RARA fusion gene

Further blood investigation results: Flow test - forward scatter: side scatter and CD45 gating. Immunophenotypic analysis performed on a sample revealed a population of 95-96% large complex cells which fall within the granulocyte gate. They showed features in keeping with acute myeloid leukaemia with features compatible with acute promyelocytic leukaemia. This case is positive (60% of screened cells) for the translocation of t(15;17)(q24;21), PML/RARA fusion gene. This finding is consistent with the diagnosis of Acute Promyelocytic Leukaemia.

4. Discussion

While literature specifically describing new-onset haematological malignancies presenting in burn patients is limited, Keys et al demonstrated that burn patients with a prior cancer diagnosis had increased odds of developing sepsis, and those with haematological neoplasms exhibited higher odds of poor outcomes [7].

APL is characterised by a life-threatening coagulopathy driven by disseminated intravascular coagulation and hyperfibrinolysis. The treatment of APL has progressively improved over time with the introduction of ATRA plus arsenic trioxide, and long-term survival rates are achievable to at least 95% [8].

Peripheral blood smears are not routinely performed for all patients presenting to the Burn Unit with anaemia, thrombocytopaenia, or leucopaenia. In this case, it was performed due to a complicated presentation and progression in a minor burn injury.

Cytopaenias are typically proportional to the burn size and clinical course. In this instance, the marked bicytopaenia and persistent bleeding in this patient with a minor 4% TBSA burn represented a clear discordance.

The associated marked leukocytosis and elevated procalcitonin raised suspicion of sepsis as the underlying cause [9]. This rare case represents a unique and challenging diagnosis in a burn patient, with many confounding signs and symptoms that, in the context of burns, would typically not be attributed to malignancy, but to wound sepsis. This raises the question of whether earlier identification of APL could have been possible within the Burns Unit where the index of suspicion for acute onset haematological malignancy is low as compared to skin malignancy transformation of chronic burns (Marjolin’s ulcers) which is also rare in the acute setting [10].

5. Conclusions

Persistent derangements in blood counts should prompt thorough investigation, without anchoring to sepsis; however, this needs to be balanced against the prevalence of sepsis-related complications in burn patients and the practical limitation of extensive investigations in resource-limited settings. This case aims to raise awareness for exploring holistic management of burn patients who present with a burn wound with complications not fully explained by the burn severity.

Patient outcomes may be improved through the development and implementation of standardised protocols for the management of cytopaenias in burn patients who demonstrate an inadequate response to conventional therapy to explore other pathology. This includes structured approaches to anaemia and thrombocytopaenia refractory to transfusions, leukopaenia not responding to antimicrobial therapy, and the incorporation of peripheral blood smear analysis to guide diagnostic evaluation and management.

Further research focusing on burn patients with underlying malignancy, particularly new-onset leukaemia, is required