Neonatal Wet Gangrene With Early Auto‐Amputation in a Resource‐Limited Setting With Incomplete Etiologic Workup: A Case Report

ABSTRACT

Neonatal limb gangrene with auto‐amputation is rare and often idiopathic. Early recognition, prompt referral, and thorough etiologic workup—despite resource limitations—are critical. Wet gangrene requires broad‐spectrum antibiotics, wound care, and timely surgical amputation to preserve growth plates and allow future prosthesis fitting.

Abbreviations

A. baumannii

Acinetobar baumannii

ANC

antenatal care

APTT

Activated partial Thromboplastin time

INR

international normalizing ratio

MCH

Mean corpuscular hemoglobin

MCHC

Mean corpuscular hemoglobin concentration

MCV

mean corpuscular volume

P. aeruginosa

Pseudomonas aeruginosa

PT

prothrombin time

WBC

white blood cell

1. Introduction

Neonatal peripheral gangrene is an uncommon event, and when it does occur it almost always follows an identifiable insult. In neonates, gangrene is usually linked to conditions such as sepsis, severe dehydration, maternal diabetes, perinatal asphyxia, or congenital coagulation defects [1]. Reported series of neonatal thrombosis have predominantly involved critically ill infants with known risk factors (e.g., indwelling catheters, infection) rather than healthy term neonates [2]. A multicenter NICU study found neonatal venous thrombosis was strongly associated with bloodstream infection and maternal diabetes [2]. By contrast, congenital gangrene of a limb is “extremely rare”, and truly idiopathic limb gangrene with auto‐amputation in a well newborn has been reported only anecdotally [3]. The present case—a term neonate with “wet gangrene” of a lower limb leading to auto‐amputation—is therefore highly unusual. We present it to underscore that severe limb ischemia can arise in neonates even without obvious precipitating factors, highlighting the need to recognize this scenario and investigate its underlying mechanisms.

1.1. Case History/Examination

The neonate was born to a 25‐year‐old primipara mother after 9 months of pregnancy. The mother had regular antenatal care (ANC) at a nearby health center and there was no problem detected during pregnancy. The labor was spontaneous and delivery was also at the same health center and it was uneventful. The duration of labor lasted 8 h and rupture of membrane was 3 h. Fetal presentation was cephalic and no birth complication was reported. The mother had no fever or foul‐smelling vaginal discharge during delivery. She wasn't diagnosed with hypertension, diabetes, or any other chronic illness. The neonate was sent home with his mother after 6 h of delivery.

At the age of 3 days, this female newborn started to develop a darkish skin color change over the right lower anterolateral leg, which then started to swell and became an open wound. For this reason, the mother took her to a nearby health center, where she was given paracetamol syrup and nitrofurantoin cream to be applied over the lesion. Despite this, the wound started to have purulent discharge, for which the mother revisited the health center after 4 days as there was no improvement but was told to continue to apply the same cream, despite the fact that the wound was expanding proximally and circumferentially up to the level of the proximal leg. Discharge from the wound later became foul smelling, and 4 days later (on the 12th day after birth), the same leg suddenly fell off at the level of the knee joint, leaving both bones of the leg exposed below the knee, as shown in Figure 1, while the mother was bathing the baby, after which she visited a primary hospital, from where she was referred to our hospital.

FIGURE 1.

Clinical photograph of the newborn's right lower limb following auto‐amputation at the level of the proximal leg. The image shows the exposed distal ends of the tibia and fibula, with complete loss of the foot and soft tissue circumferentially below the knee. The knee joint itself appears preserved. The wound edges and remaining stump show signs of moist, necrotic tissue with associated purulent discharge.

Up on physical examination the baby was stable and had no vital sign derangement. Her weight was = 3150 g, Head Circumference = 35.5 cm, oxygen saturation 96%, Pulse Rate of 164 beat/min, Temperature 36.7°C, Respiratory rate 50 breath/min. Musculoskeletal examination revealed exposed (degloved) right tibiofibular bones up to the level of proximal leg with lost foot at ankle joint sparing the right knee joints. There is circumferentially amputated skin and muscle of right leg at proximal leg as shown on the picture below (Figure 1). The distal right lower limb had already spontaneously detached, making assessment of the dorsalis pedis and posterior tibial pulses on the affected side impossible; however, palpable and strong pulses were present at the right popliteal and more proximal right leg arteries, and all palpable arteries of the left lower limb were strong with no clinical evidence of ischemia. There was also foul smelling minimal purulent discharge from the wound (Figure 1). Other systemic examinations were unremarkable.

Up on Investigations with Complete blood count, WBC‐ 17.21 × 10³/uL, Hg‐ 12.5 g/dL (Table 1). Bacterial culture was done from discharge and showed mixed colony growth on MacConkey agar (1 lactose fermenter which was identified as E. coli and 2 non‐lactose fermenter gram‐negative rods which were most likely P. aeruginosa / A. baumannii but not confirmed). Antimicrobial susceptibility test was performed and only meropenem was effective for both isolates. Further investigations like Doppler ultrasound of the limb were not done due to unavailability in our setup. After admission the child was evaluated by an orthopedic surgeon, and was given wound care and dressing while waiting for knee disarticulation.

TABLE 1.

Serial representation of serological investigations conducted from the date of admission till date of discharge.

CBC variables	Day‐1	Day‐5	Day‐15	Reference
WBC count (103/uL)	17.21	15.3	13	9.1–34
Hematocrit (%)	38	38.9	38.5	44–70
Hemoglobin (g/dL)	12.5	13	12.7	15–24
MCV (fl)	97.5	99.3	99	99–115
Plt count (103)	165	201	198	84–478
ESR (mm/h.)	15	11	11	0–17
Creatinine (mg/dl)	1.1	0.93	1.02	0.6–1.2
Blood urea nitrogen (mg/dl)	2.6	1.6	10.3	3–12
Sodium (mmol/L)	135	142	140	133–146
Potassium (mmol/L)	3.53	4.9	3.9	4.6–6.7
Chloride (mmol/L)	100	97.3	102	100–117
Calcium (mg/dl)	2.401	2.1	2.3	1.5–2.9
AST (IU/L)	43	22.6	67	35–150
ALT (IU/L)	65	71.9	57	6–50
ALP (IU/L)	195	124.66	164.3	150–420
Random blood sugar (mm\g/dl)	220	114.26	100	50–90
Prothrombin time (sec)	10.1	10.9	11.3	10.6–16.2
APTT (sec)	100.2	29.3	39.6	32–54
INR	0.84	0.9	0.91	1.1–1.7
Fibrinogen (mg/dL)	150			125–300
hsCRP (mg/L)	> 5	0.3	0.7	0.8–15.8
Blood cultures, from discharge, for aerobic, anaerobic, and fungal organisms.	Mixed colony growth on MacConkey agar (1 lactose fermenter which was identified as E. coli and 2 non‐lactose fermenter gram negative rods which was most likely P. aeruginosa/A. baumannii but not confirmed). Both isolates were sensitive only for meropenem.

Abbreviations: ALP, Alkaline Phosphatase; ALT, Alanine Transaminase; APTT, Activated Partial Thromboplastin Time; AST, Aspartate Transaminase; CBC, Complete Blood Count; ESR, Erythrocyte Sedimentation Rate; hsCRP, High‐sensitivity C‐Reactive Protein; INR, International Normalized Ratio; MCV, Mean Corpuscular Volume; Plt, Platelet; WBC, White Blood Cell.

1.2. Differential Diagnosis

The leading competing diagnoses for this neonate's progressive distal limb necrosis were (1) an infective necrotizing soft‐tissue process (wet gangrene/necrotizing fasciitis), (2) an acute arterial occlusive event (iatrogenic or thrombotic arterial thrombosis), and (3) a coagulopathy‐driven microvascular thrombosis such as purpura fulminans; less likely alternatives included congenital amniotic‐band constriction and an extravasation/chemical injury. Wet gangrene/necrotizing soft‐tissue infection was considered the most probable diagnosis because of the clinical course of rapidly progressive local tissue destruction with foul purulent discharge and a positive wound culture for gram‐negative organisms—findings that are well described in neonatal necrotizing fasciitis and polymicrobial wet gangrene.

An iatrogenic or catheter‐related arterial thrombosis (classically after umbilical or peripheral arterial cannulation) remained an important competing diagnosis because such occlusive events produce sudden distal ischemia and dry gangrene and are a frequent, reversible cause of neonatal limb loss when present; review of delivery and postnatal records for any vascular access is therefore essential. Purpura fulminans/DIC from overwhelming sepsis or congenital anticoagulant deficiency was also entertained because it can cause rapidly progressive cutaneous microvascular thrombosis and hemorrhagic necrosis in neonates; however, the patient's normal coagulation profile (normal PT/INR, aPTT, fibrinogen and platelets at evaluation) and the focal, culture‐positive limb infection argue against fulminant systemic DIC as the primary driver in this case. Amniotic‐band constriction, which causes true in utero mechanical ischemia and can result in congenital auto‐amputation, was considered unlikely given the delayed onset of lesions (day‐3 presentation) and the absence of congenital constriction rings or prenatal ultrasound findings, although it remains a diagnostic consideration when anomalies are present at birth.

Finally, extravasation or peripheral IV‐related chemical injury can produce focal necrosis in hospitalized neonates and may be complicated by secondary infection, but this was considered unlikely here in the absence of reported infusion/IV access at the affected site; nevertheless, a careful review of any peripheral line use is warranted because early recognition materially alters management.

In summary, the combination of (i) focal, rapidly progressive purulent necrosis with gram‐negative wound growth, (ii) onset after birth without documented arterial instrumentation, and (iii) a normal coagulation panel makes primary necrotizing bacterial soft‐tissue infection with secondary tissue necrosis the most likely diagnosis in this infant, with arterial thrombosis and purpura fulminans remaining important but less likely competing alternatives until Doppler vascular imaging and targeted hematologic testing exclude them.

1.3. Treatment, Outcome and Follow‐Up

Broad spectrum antibiotic was started with ceftriaxone, metronidazole, and gentamycin until culture and sensitivity arrived. After culture and sensitivity results were received, meropenem was started at 20 mg/kg IV every 8 h on day 3 of admission and was continued for a total of 10 days. The neonate's condition was stable, and she was put on daily wound care. Later on, the patient was scheduled for elective operation, and below‐knee disarticulation was done as shown on Figures 2 and 3.

FIGURE 2.

Intraoperative photograph of the newborn's right lower limb during the surgical below‐knee disarticulation. The image shows the surgical field with a clean, circumferential incision through the soft tissues of the proximal leg. The distal ends of the tibia and fibula are cleanly transected. The knee joint capsule and patella are visualized proximally and appear to be preserved. The surgical wound edges are sharp and without signs of active infection or necrosis at this stage of the procedure.

FIGURE 3.

Post‐operative photograph of the newborn's right lower limb following surgical below‐knee disarticulation. The image shows a clean, well‐approximated surgical stump at the distal thigh/proximal knee region. The wound is closed, with the residual limb forming a conical shape suitable for future prosthetic fitting. The skin appears intact without signs of acute infection, redness, or discharge. The preserved knee joint allows for potential flexion and extension, which is crucial for future mobility and rehabilitation.

The baby stayed 15 days in the hospital on antibiotic and wound care daily. There was no complication after operation and was discharged with appointment at follow up clinic for further management with prosthesis and growth assessment. The family didn't come on their initial follow up time due to financial reason but later came after 5 months of operation, and during their follow up visit the baby was well looking appearance, clean wound sight (Figure 4), and no new complaint is mentioned by family.

FIGURE 4.

Clinical photograph taken 5 months postoperatively during a follow‐up clinic visit. The image shows the healed surgical stump of the right lower limb. The residual limb maintains a healthy, well‐contoured shape with mature scar tissue at the distal end. The skin over the stump appears intact, healthy, and without signs of infection, breakdown, or inflammation. The preserved right knee joint demonstrates apparent good alignment and is held in a flexed position, suggesting maintained mobility and integrity crucial for future prosthetic rehabilitation. The overall presentation indicates successful wound healing and a functionally promising anatomical foundation for prosthetic fitting.

2. Discussion

Neonatal wet gangrene represents an acute ischemic necrosis of soft tissue in the newborn that is complicated by secondary infection and progressive liquefaction. In contrast to dry gangrene, it is characterized by edema, bacterial colonization, and a systemic inflammatory response. The development of early auto‐amputation reflects complete vascular occlusion and irreversible tissue death, with spontaneous separation occurring after formation of a clear demarcation line between viable and nonviable tissue.

Peripheral gangrene in neonates is rare, and its true incidence remains uncertain because most available data derive from case reports and small case series. Reported predisposing factors include sepsis, disseminated intravascular coagulation (DIC), umbilical arterial catheterization, polycythemia, maternal diabetes, congenital heart disease, and inherited or acquired hypercoagulable states. In limited‐resource settings, additional contextual factors such as unsupervised home deliveries, delayed access to healthcare facilities, and limited laboratory support may contribute to advanced presentation and restrict etiologic evaluation. Other associated conditions include prematurity, dehydration, prolonged tourniquet application, tight bandaging or casting, pregnancy‐induced hypertension, and maternal diabetes. Nevertheless, in a substantial proportion of cases, no clear predisposing factor can be identified and the etiology remains idiopathic [4, 5]. A review by Turnpenny et al. involving 56 neonates reported up to 1992 who presented with peripheral ischemia and gangrene at or shortly after birth found that no definite etiology could be established in the majority of cases [4]. Similarly, Kothari et al. [6] described four neonates with bilateral lower limb gangrene requiring amputation; two had undergone exchange transfusion, while in the remaining two no cause was identified. Nagai et al. [7] reported two cases of intrauterine bilateral lower limb gangrene associated with prematurity and twin‐to‐twin transfusion syndrome, both necessitating below‐knee amputation. Collectively, these reports underscore that the precise mechanism underlying peripheral limb ischemia and gangrene in neonates presenting at or soon after birth frequently remains unclear.

The pathophysiology of neonatal limb ischemia and gangrene likely reflects a complex interplay between developmental hemostasis, endothelial injury, and inflammatory activation. Neonates exhibit physiologically reduced levels of several procoagulant and anticoagulant proteins—including protein C, protein S, and antithrombin compared with older children [8]. This developmental hemostatic balance renders them particularly vulnerable to perturbations. Infectious insults, especially Gram‐negative sepsis, can shift this balance toward a prothrombotic state. Lipopolysaccharide (LPS) triggers monocyte and neutrophil activation with release of proinflammatory cytokines (e.g., TNF‐α, IL‐1, IL‐6), which upregulate tissue factor expression on endothelial cells and leukocytes [9]. Concurrently, these cytokines impair natural anticoagulant pathways by downregulating thrombomodulin and endothelial protein C receptor expression, thereby reducing protein C activation. In neonatal sepsis, protein C levels may decline precipitously, predisposing to DIC and purpura fulminans [9]. The resultant microvascular thrombosis can lead to occlusion of small vessels in the skin and distal tissues, manifesting as symmetrical peripheral gangrene or rapidly progressive skin necrosis. Both Gram‐positive and Gram‐negative organisms, including Staphylococcus, Streptococcus, Klebsiella, and Escherichia coli , have been implicated in this process. Thus, severe infection and endotoxemia may induce endothelial injury and micro thrombosis culminating in localized gangrene [10].

Two principal mechanisms may explain limb gangrene in the present patient. The first involves a primary necrotizing soft‐tissue infection, potentially caused by a Gram‐negative bacillus, leading to local endothelial injury and activation of coagulation pathways. In this model, endotoxin‐mediated cytokine release promotes intravascular thrombosis within the limb microcirculation, resulting in infected (“wet”) gangrene [9, 10]. Evidence from neonatal purpura fulminant supports the plausibility of infection‐induced intravascular coagulation and limb necrosis in the absence of large‐vessel obstruction. The alternative hypothesis is primary arterial occlusion such as an intrauterine thrombus or embolus causing ischemia followed by secondary infection [2]. However, isolated neonatal arterial thrombosis is typically associated with identifiable risk factors, including umbilical catheterization, maternal hypertension, or growth restriction, none of which were present in this case. In the absence of imaging or histopathological confirmation, the exact sequence cannot be determined. Nonetheless, the predominance of infectious features and the lack of profound systemic cardiovascular compromise favor an infection‐triggered microthrombotic process over primary large‐vessel occlusion.

Management of neonatal wet gangrene is largely supportive and guided by the extent of ischemia and infection. Initial therapy includes broad‐spectrum systemic antibiotics, meticulous local wound care, and, in selected cases, the use of systemic or topical vasodilators [11]. Early surgical intervention is warranted when ischemic changes are severe or progressive. However, in many instances, spontaneous sloughing or auto‐amputation occurs after a demarcation line becomes evident. Surgical amputation should ideally be deferred until a clear demarcation between viable and nonviable tissue has developed to avoid unnecessary loss of healthy tissue. When amputation is required, surgical planning must prioritize preservation of the growth plate and creation of an adequate stump to facilitate future prosthetic fitting and functional rehabilitation. In the present case, a below‐knee amputation was performed with these principles in mind [12].

In summary, neonatal peripheral limb gangrene is an uncommon but serious condition with multifactorial and often elusive etiology. A comprehensive evaluation is essential to identify underlying causes, guide management, and inform prognosis. Although infectious and micro‐thrombotic mechanisms appear highly plausible in many cases, definitive conclusions are frequently limited by diagnostic constraints, underscoring the need for further systematic investigation.

2.1. Strengths and Limitations

This report's strengths include a detailed clinical timeline, microbiologic evidence of polymicrobial gram‐negative infection, clear photographic documentation of the lesion and surgical outcome, and documented medium‐term follow‐up demonstrating a satisfactory stump and recovery despite socioeconomic barriers. The study's main limitations are the incomplete etiologic workup inherent to a resource‐limited setting: no arterial Doppler/angiography was performed to document vessel patency or level of occlusion, no thrombophilia panel (protein C/S, antithrombin, factor V Leiden, prothrombin mutation, antiphospholipid antibodies) or echocardiography was obtained to exclude embolic or congenital cardiac sources, and detailed maternal/placental evaluation (including diabetes, hypertensive disorders, or placental pathology) was not available. Histopathological examination of the amputated tissue was not performed, limiting definitive demonstration of fascial/myonecrosis or thrombotic occlusion. Given these gaps, the case should be described as neonatal lower‐limb gangrene of undetermined etiology rather than definitively “idiopathic.” Future similar cases should include vascular imaging, targeted hematologic testing, echocardiography, and maternal/placental assessment when feasible to clarify pathogenesis and guide management.

2.2. Learning Points

• Auto‐amputation can occur suddenly in neonatal wet gangrene even without identified vascular or thrombotic risk factors

• In resource‐limited settings, advanced investigations (Doppler, thrombophilia workup) may be unavailable, necessitating careful clinical monitoring and early surgical referral.

• Broad‐spectrum antibiotics and daily wound care are essential while awaiting culture results and demarcation for amputation.

• Surgical amputation in neonates should aim to preserve growth plates and ensure an adequate stump for future prosthetic rehabilitation.

• Parent counseling and follow‐up are crucial, as socioeconomic factors may affect adherence to postoperative care and prosthesis planning

Author Contributions

Milki Tufa Feyisa: conceptualization, data curation, investigation, methodology, resources, software, validation, visualization, writing – original draft, writing – review and editing. Beza Eshetu: writing – original draft, writing – review and editing. Tolosa Dibisa: writing – original draft, writing – review and editing. Mulatu Gshaw: writing – original draft, writing – review and editing. Birhanu Tolera: conceptualization, resources, software, supervision, validation, visualization, writing – original draft, writing – review and editing. Endalew Dessie Birara: writing – original draft, writing – review and editing. Adugna Lamessa: methodology, validation, visualization, writing – original draft, writing – review and editing. Tamirat Godebo Woyimo: conceptualization, data curation, methodology, resources, software, validation, visualization, writing – original draft, writing – review and editing.

Funding

The authors have nothing to report.

Ethics Statement

Ethical approval for publication of this case report, including use of clinical data and accompanying images, was obtained from the Jimma University Institutional Review Board (IRB). The IRB reviewed the case and approved publication in accordance with institutional policies and international ethical standards (Declaration of Helsinki).

Consent

Written informed consent for publication of the clinical details and all clinical images was obtained from the patient's parent/legal guardian. The parent/legal guardian received an information sheet explaining the purpose of publication, the types of clinical data and images that would be shared, and the measures taken to protect confidentiality (removal of personal identifiers and cropping/obscuring of distinguishable features where needed). The parent/legal guardian agreed to publication and signed the consent form prior to manuscript submission. All patient identifiers have been removed from the manuscript to preserve anonymity.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

All the information used to describe the case is within the article.