CASE 17749 Published on 10.06.2022

Imaging of hypovolemic shock in polytrauma beyond the cause: The CT Hypoperfusion Complex


Abdominal imaging

Case Type

Clinical Cases


Susmitha Garudadri, Anusha Sambangi, Puligunta Pooja Nikhitha

GSL Medical College, Rajahmundry Andhra Pradesh, India


18 years, male

Area of Interest Abdomen, Arteries / Aorta, Kidney, Liver, Musculoskeletal bone, Veins / Vena cava ; Imaging Technique CT, Digital radiography, Ultrasound
Clinical History

An 18-year-old male presented to emergency department with an alleged history of road traffic accident in an unconscious and hemodynamically unstable state with a Glasgow coma score of 3. Primary survey revealed traumatic brain injury, blunt trauma to the abdomen with soft tissue and bone injuries.

Imaging Findings

Radiographic imaging revealed compound fracture of right distal femur (Fig 1), Shaft of the left tibia (Fig 2), pubic diastasis (Fig 3)

Ultrasound abdomen showed liver contusion (Fig 4) with minimal hemoperitoneum.

CECT [Contrast Enhanced Computed Tomography] abdomen showed Grade-2 liver injury with contusion (Fig 5), hypo enhancing spleen (Fig 5), mild hemoperitoneum (Fig 6), flattened IVC [Inferior vena cava] (Fig 5&7), hyper enhancing small bowel walls with mucosal thickening (Fig 8), hyper enhancing adrenals (Fig 9), heterogenous pancreas with peri pancreatic fluid (Fig 5&10).

CT Pelvis revealed un displaced fracture of right superior and inferior pubic rami and left ala of sacrum, pelvic hematoma, inflammation of the anterior abdominal muscles at the level of pelvis.

CT Brain showed left tentorial SAH, haemorrhage in occipital horns of bilateral lateral ventricles, along the interventricular septum and posterior interhemispheric falx.


This is a case of hypoperfusion complex secondary to polytrauma in a young male patient. Symptomatic management to maintain hemodynamic stability and surgical management for the fractures was done and the patient`s clinical status significantly improved over the time. CT hypoperfusion complex occurs at a higher rate in post-traumatic patients. However, shock can occur due to multiple causes like hypovolemia, trauma, sepsis, cardiac arrest, severe head injury. There are three stages of shock: compensatory, decompensatory, and irreversible. Understanding the signs of CT hypoperfusion complex prevents confusion with other pathologies like ileus, gallbladder perforation, mesenteric ischemia, portal venous thrombosis. The signs of CT hypoperfusion complex can be divided under two: vascular and non-vascular [1]. It is said that vascular signs represent the true hypovolemic state and nonvascular /visceral signs represent hypoperfusion state.[5] Low-calibrated abdominal aorta, IVC, and mesenteric arteries come under vascular signs. Dilated and edematous bowel loops, hyperdense adrenal glands, shock kidney, shock pancreas, free fluid in the abdomen, splenic and hepatic perfusion deficits, and pericholecystic fluid come under non-vascular signs. Presence of two or more vascular, visceral, or parenchymal signs is necessary to establish the presence of CT hypoperfusion complex [1].

The following can be considered as the diagnostic criteria:

  • Abdominal aorta diameter <13 mm seen 20 mm above and below the renal arteries [3]
  • For the flattening of  IVC, AP diameter has to be reduced (< 9 mm) in 3 consecutive segments, 20 mm above and below the renal veins, and at the level of  perihepatic portion.
  • Hyperdense adrenal glands seen due to adrenergic mechanisms in response  to hypovolemic shock. [1]
  • Shock kidney refers to hyperdense kidneys with delayed nephrogram.
  • In case of hypoperfused spleen and liver - relative hypo enhancement is seen[2]
  • Variable enhancement of the pancreas with peripancreatic fluid (shock pancreas)[4]
  • Shock bowel refers to luminal distention, intense mucosal hyperenhancement, mural stratification, bowel wall thickening, and intraluminal fluid. These signs occur due to sympathetic stimulation resulting in splanchnic vasoconstriction and reduction of intestinal perfusion.

Hypovolemia leads to decreased arterial inflow and venous outflow resulting in the ischemic change.[2] Acute disruption of the autoregulatory mechanisms of circulation results in adrenergic responses maintaining cardiac output and sufficient blood pressure. When compensatory measures are overcome by ongoing haemorrhage, the uncompensated state results in early ischemic changes, which can rapidly become irreversible without resuscitation.[2]. The appropriate treatment is supportive therapy rather than the surgical intervention.


The CT hypoperfusion complex can be seen in blunt trauma patients with hypovolemic shock. It offers a quick guidance in the acute trauma setting, allowing the radiologist to alert the treating physicians to a possible impending hypovolemic shock.

Differential Diagnosis List
CT Hypoperfusion Complex secondary to polytrauma
Mesenteric ischemia
Portal venous thrombosis
Gallbladder perforation
Final Diagnosis
CT Hypoperfusion Complex secondary to polytrauma
Case information
DOI: 10.35100/eurorad/case.17749
ISSN: 1563-4086