Keywords<\/h2>\n
Extremity hemorrhage, trauma, vascular injury, hypovolemic shock, massive transfusion<\/p>\n
Introduction<\/h2>\n
Hemorrhage is the leading cause of preventable mortality in trauma. While torso bleeding is commonly emphasized, extremity hemorrhage can be significant and occult, leading to delayed recognition and deterioration.<\/p>\n
Case Presentation<\/h2>\n
A 59-year-old male presented to the emergency department with an alleged history of road traffic accident (two-wheeler vs two-wheeler). He sustained injuries to head , both lower limbs and had a history of loss of consciousness and amnesia of the event. He was initially taken to an outside hospital, and details of prior management were not available.<\/p>\n
There was no history of chest pain, breathlessness, abdominal pain, or bowel and bladder disturbances.<\/p>\n
Past medical history : hepatitis B positive , Rheumatoid arthritis<\/p>\n
Past surgical history: S\/P liver transplantation (2022)<\/p>\n
Primary Survey (XABCDE)<\/h2>\n
X (Exsanguination): No active external bleeding noted. Left leg dressing was intact with no soakage.<\/p>\n
A (Airway): Airway patent. Cervical spine immobilization applied.<\/p>\n
B (Breathing): Bilateral air entry present, SpO\u2082: 98% on room air, RR: 18\/min<\/p>\n
C (Circulation): S1, S2 present, no murmur, BP: 100\/60 mmHg, PR: 76 bpm<\/p>\n
Abdomen: Soft, non-tender, bowel sounds present<\/p>\n
D (Disability): GCS: 15\/15, Pupils: Equal and reactive (2 mm), Moving all four limbs<\/p>\n
E (Exposure): Temperature: 97.6\u00b0F<\/p>\n
Adjuncts<\/h2>\n
ABG<\/p>\n
PH: 7.36
\nPCO\u2082: 32 mmHg
\nPO\u2082: 88 mmHg
\nHCO\u2083\u207b: 18.3 mmol\/L
\nBase excess: -7.3
\nLactate: 4.4 mmol\/L
\nHemoglobin: 9.5 g\/dL
\nHematocrit: 24%
\nSodium: 132 mEq\/L
\nPotassium: 3.5 mEq\/L
\nChloride: 105 mEq\/L
\nCreatinine: 1.4 mg\/dL
\nECG: Normal sinus rhythm, no acute ST-T changes<\/p>\n
EFAST:<\/p>\n
B\/L lung sliding present
\nNo pneumothorax or hemothorax
\nCardiac contractility : adequate no cardiac tamponade<\/p>\n
No free fluid in hepatorenal and splenorenal angle
\nBladder normal.<\/p>\n
Secondary Survey<\/h2>\n
head-to-toe examination revealed:<\/p>\n
Head & Face: Forehead: abrasion of 3x3cm above the right eyebrow.
\nNeck: No tenderness or swelling
\nChest: Bilateral air entry equal, no tenderness
\nAbdomen: Soft, non-tender, no distension
\nPelvis: Stable
\nSpine: No deformity or tenderness
\nExtremities<\/p>\n
Left Lower Limb:<\/strong><\/p>\n Deep laceration (~20 \u00d7 5 \u00d7 10 cm) over anterolateral aspect of lower leg Right Lower Limb:<\/strong><\/p>\n Knee swelling + XRAY for B\/L lower limb ordered<\/p>\n Upon awaiting for radiological imaging Patient developed hypotension<\/p>\n On reassessment:<\/strong><\/p>\n Blood pressure dropped to 70\/40 mmHg Patient shifted for PAN-CT \u2013 TRAUMA PROTOCOL<\/p>\n X-rays:<\/strong><\/p>\n Right knee: Proximal tibia fracture<\/p>\n Left ankle: Compound trimaleolar ankle fracture<\/p>\n Identification of Bleeding Source : With no torso source identified: upon exploration of left leg<\/p>\n Active oozing observed At this point BP :90\/60 mm hg\/ PR: 90 bpm, on ongoing PRBC transfusion.<\/p>\n IMPRESSION:<\/strong>\u00a0 Compound trimaleolar fracture left ankle with Vascular injury<\/p>\n DIFFINITIVE MANAGEMENT<\/strong>: <\/strong>Patient shifted to OT with ongoing resuscitation.<\/p>\n Postoperatively, the patient remained hemodynamically stable with satisfactory clinical recovery and was discharged in a stable condition on day 7.<\/p>\n This case highlights a critical and often under-recognized cause of traumatic shock\u2014occult extremity hemorrhage leading to delayed exsanguination despite an initially stable presentation. While trauma protocols traditionally emphasize thoracic, abdominal, and pelvic sources of bleeding, this case reinforces that extremities can serve as a significant and potentially fatal reservoir of blood loss, particularly in the presence of deep soft tissue and vascular injury.<\/p>\n A key teaching point illustrated here is the fundamental trauma principle that \u201cin trauma, shock must be presumed hemorrhagic until proven otherwise.\u201d In this patient, the absence of active external bleeding, combined with a negative EFAST and unremarkable torso imaging, initially suggested hemodynamic stability. However, the subsequent development of hypotension with elevated lactate and base deficit indicated ongoing occult hypoperfusion. This underscores that early clinical findings may be deceptively reassuring, and reliance on a single-point assessment can delay recognition of life-threatening hemorrhage.<\/p>\n The pathophysiology of delayed bleeding in this case is multifactorial. Initial hemostasis may have been achieved through temporary tissue tamponade and unstable clot formation within the deep muscular compartments of the leg. Subsequent resuscitation, along with patient handling and interdepartmental transfers, may have contributed to clot dislodgement, converting a contained hematoma into active hemorrhage. This phenomenon is well described in trauma but remains underappreciated in routine clinical practice. Therefore, any clinical deterioration following patient movement should prompt immediate reassessment of previously identified injuries.<\/p>\n Another important aspect is the dynamic nature of vascular injuries. The initial presence of distal pulses in this patient likely reflected collateral circulation or partial arterial injury, which masked the severity of vascular compromise. The later loss of distal pulses was a crucial clinical sign that prompted further evaluation. This highlights that the presence of distal pulses does not exclude significant vascular injury, and serial neurovascular examinations are essential in extremity trauma.<\/p>\n This case also emphasizes the limitations of imaging modalities in early trauma assessment. Both EFAST and PAN-CT failed to identify a bleeding source. Notably, the PAN-CT protocol in our setting included imaging only up to the mid-thigh and did not cover distal extremities, thereby potentially missing vascular injuries below this level. Additionally, the hemorrhage was localized and confined within soft tissue compartments without significant accumulation detectable on imaging. This highlights that negative imaging does not exclude ongoing hemorrhage, particularly in extremity trauma, and reinforces that clinical judgment and repeated bedside reassessment remain paramount in identifying evolving bleeding sources.<\/p>\n The timely activation of the massive transfusion protocol (MTP) played a pivotal role in this patient\u2019s survival. Early balanced transfusion (1:1:1 ratio) helps mitigate trauma-induced coagulopathy, restore circulating volume, and improve oxygen delivery. Importantly, this case reinforces that MTP should be initiated based on clinical suspicion rather than delayed until definitive identification of the bleeding source.<\/p>\n From a systems perspective, this case underscores the importance of a multidisciplinary approach, involving emergency physicians, orthopedic surgeons, vascular surgeons, and plastic surgeons. Early coordination allowed for definitive surgical control of bleeding, including vascular ligation and fracture stabilization, which ultimately resulted in a favorable outcome.<\/p>\n Several key learning points emerge from this case:<\/p>\n This case reinforces that occult extremity hemorrhage is a potentially fatal yet preventable cause of delayed shock in trauma patients. Emergency physicians must maintain a high index of suspicion, particularly in patients with unexplained hypotension and negative torso imaging. Ultimately, vigilant serial reassessment, early resuscitation, and prompt surgical intervention remain the cornerstones of successful trauma management.<\/p>\n Dr. Avinash S
\nMuscle exposure noted
\nNo active bleeding
\nRestricted ankle movement
\nPainful knee movement
\nDistal pulses \u00a0+<\/p>\n
\nTenderness+
\nROM Restricted and painful
\nCrepitus present
\nDistal pulses palpable
\nNo additional injuries were identified.<\/p>\nInitial management in ED<\/h2>\n
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Clinical Course<\/h2>\n
\nRepeat EFAST: No new findings
\nIVC: Collapsible
\nIntervention
\nFluid resuscitation initiated
\nMassive transfusion protocol (1:1:1) activated
\nNoradrenaline infusion started<\/p>\n\n
\nMinimal subarachnoid hemorrhage<\/li>\n
\nIncidental cholelithiasis<\/li>\n![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2026\/05\/proximal-tibia-fracture.jpg\")
<\/figure>\n![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2026\/05\/compound-trimaleolar-ankle-fracture.jpg\")
<\/figure>\nClinical Deterioration<\/h1>\n
\nWound packed and compressed
\nNew finding: Distal pulse became absent
\nAn urgent vascular opinion obtained<\/p>\n\n
![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2026\/05\/ct-peripheral-angiography.jpg\")
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OUTCOME:<\/h2>\n
Discussion<\/h2>\n
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Conclusion<\/h2>\n
References<\/h2>\n
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![\"\"](\"https:\/\/www.kauveryhospital.com\/ima-journal\/wp-content\/uploads\/2024\/12\/dr.avinas.jpg\")
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\nDepartment of Emergency Medicine,
\nKauvery Hospital, Alwarpet, Chennai.<\/a><\/b><\/p>\n<\/div>\n<\/div>\n
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