Spontaneous Splenic Laceration in Plasmodium falciparum Malaria: A Case Report

Introduction

Malaria remains a major cause of morbidity and mortality in endemic regions, with Plasmodium falciparum responsible for the most severe manifestations.^1,2 The spleen plays a key role in filtering parasitized erythrocytes and mounting an immune response. During acute infection, pathological changes such as congestion, cellular hyperplasia, and increased friability predispose the spleen to injury.^1,3

Splenic rupture is a recognized but uncommon complication of malaria.^4,5 In contrast, splenic laceration without complete rupture or associated with multifocal infarction is less frequently reported and may be overlooked clinically.^6,7 Such cases can present as an acute abdomen and require prompt diagnosis and management to prevent life-threatening hemorrhage. We present a case of spontaneous splenic laceration secondary to P. falciparum malaria requiring emergency splenectomy. ⁸

Case Presentation

Diagnostic Assessment

Laboratory investigations (Table 1) revealed a white blood cell count of 26.7 × 10s/µL, severe anemia with a hemoglobin of 5.1 g/dL, and a platelet count of 108 × 10s/µL. Peripheral blood smear confirmed Plasmodium falciparum infection. Renal function was mildly impaired (Creatinine 1.5 mg/dL), and inflammatory markers were elevated (CRP 176.1 mg/L).

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Table 1.

Laboratory Investigations on Admission

Investigation	Result	Reference range	Units
White Blood Cell (WBC)	26.7	4.0 – 11.0	× 10s/µL
Neutrophils	69.7	40 – 75	%
Lymphocytes	14.3	20 – 45	%
Hemoglobin (HGB)	5.1	13.5 – 17.5	g/dL
Hematocrit (HCT)	12.3	41 – 53	%
Mean Corpuscular Volume (MCV)	83.6	80 – 100	fL
Platelet Count (PLT)	108	150 – 450	× 10s/µL
Blood Group	A+	-	-
Blood Film (BF)	P. falciparum	Negative	-
Prothrombin Time (PT)	16	11 – 13.5	seconds
Partial Thromboplastin Time (PTT)	31.3	25 – 35	seconds
INR	1.33	0.8 – 1.2	-
Sodium (Na+)	125.3	135 – 145	mmol/L
Potassium (K+)	3.58	3.5 – 5.0	mmol/L
Chloride (Cl-)	109.8	98 – 107	mmol/L
Calcium (Ca2+)	1.01	2.1 – 2.6	mmol/L
Total Bilirubin (TB)	3.61	0.1 – 1.2	mg/dL
Direct Bilirubin (DB)	0.78	0.0 – 0.3	mg/dL
Serum Creatinine	1.5	0.6 – 1.2	mg/dL
C-Reactive Protein (CRP)	176.1	< 10	mg/L
Amylase	272	30 – 110	U/L
Lipase	72	0 – 160	U/L

A diagnostic abdominal tap yielded non-clotting hemorrhagic fluid. Contrast-enhanced abdominopelvic computed tomography (CT) revealed a high-grade splenic injury (AAST Grade IV) characterized by multifocal splenic infarctions, a large perisplenic hematoma, and involvement of the splenic hilum (Figure 1). Significant hemoperitoneum was noted, although no active contrast extravasation (blush) was identified at the time of imaging.

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Figure 1.

Contrast-enhanced CT of the abdomen. Axial view showing multifocal areas of low attenuation within the splenic parenchyma consistent with infarctions (white arrows) with a large perisplenic hematoma and free intraperitoneal fluid indicating hemoperitoneum

Therapeutic Intervention, Outcome, and Follow-Up

Due to progressive hemodynamic instability (persistent tachycardia and falling blood pressure) and signs of spreading peritonitis, the patient underwent emergency exploratory laparotomy.

Intraoperative findings confirmed approximately 2000 mL of hemolyzed blood in the general peritoneum. A massive splenic laceration was identified on the splenic surface extending into the hilar area (Figure 2).

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Figure 2.

Gross specimen of the ruptured spleen. Diaphragmatic surface showing multiple deep lacerations and areas of subcapsular hemorrhage

A total splenectomy was performed. The procedure involved ligation of the splenic artery, splenic veins, and short gastric vessels. The splenic phrenic, splenic renal, and splenic gastric ligaments were released to facilitate removal. Hemostasis was secured, and the abdomen was lavaged thoroughly. A left subphrenic drain was left in situ. The patient remained stable intraoperatively and received two units of whole blood.

Postoperatively, the patient was managed in the intensive care unit (ICU) for three days. He received an additional unit of blood in the ICU. His postoperative laboratory results showed a WBC of 4.5 × 10s/µL, Hgb of 9.7 g/dL, and a platelet count of 145 × 10s/µL. Antimalarial therapy was continued with intravenous artesunate, followed by a full course of oral artemether-lumefantrine.

To prevent overwhelming post-splenectomy infection (OPSI), the patient received vaccinations against Streptococcus pneumoniae, Haemophilus influenzae type b, and Neisseria meningitidis on postoperative day 7. He was also started on prophylactic penicillin V and educated on the lifelong risk of OPSI and the need for prompt medical attention for any febrile illness.

At follow-up four weeks after discharge, the patient remained clinically stable with no recurrent abdominal symptoms, fever, or evidence of infectious complications. The surgical wound had healed well, and the patient reported adherence to antimalarial treatment and prophylactic measures following splenectomy. He was counseled regarding the lifelong risk of OPSI and the importance of seeking prompt medical attention for febrile illnesses.

Discussion

Splenic complications in malaria are uncommon but potentially life-threatening, arising from a combination of reticuloendothelial hyperplasia, vascular congestion, and increased intrasplenic tension.^1,9 These pathological changes render the spleen fragile and susceptible to injury even in the absence of trauma.^1,10

While splenic rupture is the most frequently reported complication, this case is notable for several distinguishing features. First, the patient demonstrated a high-grade splenic injury (AAST Grade IV) characterized by multifocal splenic infarctions and hilar involvement. This pattern suggests that vascular occlusion and segmental ischemia may play a central role in splenic injury in falciparum malaria.^6,7 The transition from infarction to laceration and subsequent hemorrhage likely represents a continuum of splenic pathology in severe malaria, where ischemic tissue becomes increasingly friable and prone to structural failure.

Second, despite the absence of contrast extravasation on CT, the patient developed clinically significant hemoperitoneum and hemodynamic deterioration. This highlights an important diagnostic challenge: the absence of active bleeding on CT does not exclude severe or progressive splenic injury. In resource-limited settings, reliance solely on imaging findings may delay life-saving intervention.^11,12 The decision for surgery should be guided primarily by the clinical status and hemodynamic trends of the patient.

Third, this case underscores the difficulty in differentiating between splenic infarction, laceration, and impending rupture in malaria. ⁶ Multifocal infarctions, as observed here, may represent an intermediate stage in the spectrum of splenic injury, progressing from vascular compromise to structural disruption and hemorrhage. ⁷ Recognition of this continuum is critical for timely decision-making.

Management of splenic injury in malaria remains controversial, particularly in hemodynamically stable patients where conservative approaches may be considered.^4,13 However, this case reinforces that high-grade injuries with vascular involvement carry a significant risk of deterioration, and early surgical intervention should be strongly considered when clinical status worsens, regardless of initial imaging findings.^10,11

Limitations

Several limitations should be acknowledged. First, this report describes a single patient, limiting the generalizability of the findings. Second, histopathological examination of the spleen was not available to further characterize the relationship between splenic infarction and laceration. Third, longer-term follow-up data were limited, restricting assessment of delayed complications following splenectomy. Finally, as with many case reports, causal relationships cannot be definitively established, and conclusions are based on clinical, laboratory, imaging, and intraoperative findings.

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