Macias-Narvaez et al. (2026)
communication barriers. Objective: To describe a d clinical case of acute leg compartment
syndrome with atypical presentation, delayed diagnosis, and functional sequelae, integrating a
narrative review of clinical assessment, diagnostic strategy, therapeutic management, and
rehabilitation. Case: A 34-year-old male presented with closed right-leg contusion after a low-
energy motorcycle accident and no initial radiographic fracture. He was initially treated as a soft-
tissue injury. Eighteen hours later, he developed progressive pain partially controlled with opioids,
dorsal foot paresthesia, increased compartment firmness, and weakness of ankle dorsiflexion.
The anterior compartment pressure was 54 mmHg and the delta pressure was 20 mmHg. Four-
compartment fasciotomy was performed 22 hours after trauma, revealing severe muscle edema
and patchy ischemic changes. Secondary debridement, negative-pressure wound therapy,
delayed closure, and split-thickness skin grafting were required. At six months, residual deep
peroneal sensory loss and mild dorsiflexion weakness persisted, with independent gait and partial
return to work. Conclusion: Acute compartment syndrome may have an atypical course with
preserved pulses, non-florid pain, or late neurologic findings. High clinical suspicion, serial
reassessment, and timely pressure measurement in equivocal cases are essential to reduce
diagnostic delay. Functional outcome depends on ischemia duration, timing of decompression,
complication control, and multidisciplinary rehabilitation.
Keywords: acute compartment syndrome; fasciotomy; delayed diagnosis; extremity trauma;
rehabilitation; atypical pain.
constrictivos complicaciones
y
1. Introducción
iatrogénicas [1,4,5].
El síndrome compartimental agudo
SCA) es una condición tiempo-
El diagnóstico continúa siendo un
reto clínico porque no existe un
patrón único capaz de confirmar o
descartar el SCA en todos los
(
dependiente que ocurre cuando la
presión dentro de un compartimento
muscular la
cerrado
supera
pacientes.
El
dolor
capacidad de perfusión capilar,
desproporcionado, el dolor con
estiramiento pasivo, la tensión
compartimental y las parestesias son
señales de alarma; sin embargo, los
generando
hipoxia,
e
edema
disfunción
isquemia
progresivo,
neuromuscular
irreversible si no se actúa de forma
urgente [1-4]. Su etiología más
signos
clásicos
pueden
ser
inespecíficos, tardíos
o
estar
frecuente
es
traumática,
ausentes en escenarios atípicos. La
presencia de pulsos periféricos no
excluye el diagnóstico, debido a que
el compromiso microvascular puede
aparecer antes de la pérdida de flujo
arterial macroscópico [2,4,6].
especialmente asociada a fracturas
de tibia, fracturas del antebrazo,
lesiones
por
aplastamiento,
traumatismos de tejidos blandos,
reperfusión posterior a isquemia,
quemaduras, vendajes o yesos
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