Multidetector CT Imaging Biomarkers in Shock: History
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Contributor:
Tullio Valente
,
Giorgio Bocchini
,
Candida Massimo
,
Gaetano Rea
,
Roberta Lieto
,
Salvatore Guarino
,
Emanuele Muto
,
Ahmad Abu-Omar
,
Mariano Scaglione
,
Giacomo Sica

A severe mismatch between the supply and demand of oxygen is the common sequela of all types of shock, which present a mortality of up to 80%. Various organs play a protective role in shock and contribute to whole-body homeostasis. The ever-increasing number of multidetector CT examinations in severely ill and sometimes unstable patients leads to more frequently encountered findings leading to imminent death, together called “hypovolemic shock complex”. Features on CT include dense opacification of the right heart and major systemic veins, venous layering of contrast material and blood, densely opacified parenchyma in the right hepatic lobe, decreased enhancement of the abdominal organ, a dense pulmonary artery, contrast pooling in dependent lungs, and contrast stasis in pulmonary veins. These findings are biomarkers and prognostic indicators of paramount importance which stratify risk and improve patient outcomes.

  • cardiogenic shock
  • computed tomography
  • contrast layering
  • venous pooling
  • hypovolemia
  • hypovolemic shock complex

1. Introduction

Shock is a life-threatening condition defined as a state of cellular and tissue hypoxia due to reduced delivery, increased consumption, inadequate utilization of oxygen, or a combination of these processes [1][2].
Shock is not a disease but a continuum of systemic derangement and the final manifestation of a complex list of etiologies [3].
The four different subgroups of shock with characteristic hemodynamic patterns assigned to four organ systems include: distributive shock (vascular system), hypovolemic shock (blood and fluids compartment), cardiogenic shock (heart), and obstructive shock-(circulatory system) (Table 1) [4][5][6][7][8][9][10][11]. It is important to distinguish between these entities since treatment is different for various underlying etiologies [12].
Table 1. Classification (causes, pathogenesis, and treatment targets) and relative incidence of various types of shock. Systemic arterial hypotension, cutaneous, renal, and neurological signs of tissue hypoperfusion and hyperlactatemia are often present in all shock pathophysiological mechanisms.

Shock

Types

Pathogenesis

Causes

Pathophysiology

Treatment Targets

Cardiogenic (13%)

Sudden impairment of myocardial performance

  • Myocardial

  • Rhytmologic

  • Mechanical

A critical reduction of the heart’s pumping capacity, a reduced ejection fraction or impaired ventricular filling

Remove the cardiac causes of the shock

Hypovolemic (27%)

Inadequate organ perfusion caused by loss of intravascular volume

  • Hemorragic (e.g., variceal bleeding)

  • Traumatic hemorragic

  • Hypovolemic in the narrower sense (e.g., diarrhea)

  • Traumatic hypovolemic (e.g., severe surface burns)

Inadequate organ perfusion caused by acute loss of intravascular volume, drop in cardiac preload to a critical level

Intravascular volume replacement, endotracheal intubation

Distributive (59%)

Hypovolemia resulting from pathological redistribution of the absolute intravascular volume

  • Septic (55%)

  • Anaphylactid/Anaphylactoid

  • Neurogenic

  • Systemic inflammatory response syndrome (SIRS)

  • Drug and Toxin-induced shock

  • Endocrine shock

Loss of regulation of vascular tone and/or disordered permeability of the vascular system

Support circulation by infusion of balanced solutions, administration of vasopressors and/or inotropic drugs, organ replacement therapy

Obstructive (1%)

RV-LV Preload ↓

RV-LV Afterload ↑

Obstruction of the great vessels or the heart

  • Classified according to the location of the obstruction in the vascular system in relation to the heart (e.g., SVCs., PE, Obstruction aortic flow)

Intravasal/Intraluminal (e.g., PE, Leriche S., AD)

Extravasal/extraluminal (e.g., Tension PNX, Tamponade)

Immediate causal treatment (e.g., thrombolysis, thoracic or pericardial drainage; surgical embolectomy)
AD, aortic dissection; LV, left ventricle; PE, pulmonary embolism; PNX, pneumothorax; RV, right ventricle; SVC, superior vena cava. ↓: reduce, ↑: increase.
Initially, the effects of shock are reversible as the body initiates compensatory responses to counteract diminished tissue perfusion. However, if the underlying cause is not effectively addressed, shock can progress to irreversible multi-organ failure and ulti-mately result in death [1][3][4][6][11][12].
When patients with undifferentiated hypotension or shock arrive at the emergency department (ED), it is crucial for the emergency physician to categorize them based on the severity of shock and determine the requirement for immediate or early intervention.
Contrast-enhanced multidetector CT (CECT) of the chest, abdomen and pelvis is increasingly required as the first line of imaging in suspected cardiovascular emergencies in severely sick and unstable patients [13]. CT may help identify the cause for shock (e.g., obstructive shock in pulmonary embolism or aortic dissection) [14]. Previous reports have predominantly focused on describing distinct imaging signs observed on CT scans, commonly referred to as the “hypovolemic shock complex” (HSC) [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. While these findings are frequently observed in patients with hemorrhagic and hypovolemic shock complex, they can also be present in individuals experiencing conditions such as myocardial infarction, sepsis, or even diabetic ketoacidosis [33].

2. Multidetector CT (MDCT) Technique

Detection of relevant CT signs must be accurate, reproducible, and feasible over time, for which a state-of-the-art CECT technique is needed. Nowadays, CT technology consists of a multidetector-spiral CT between 8- and 640-slice CT. Acquisition times and number of contrast-enhanced phases are not standardized for all CT scanners.
CECT should be performed in critical patients with a volumetric technique, with craniocaudal acquisition, in a supine position, and, when possible, preferably in a “feet first” position [34]. Breath-hold acquisition can ensure the avoidance of motion artifacts if clinical condition permits [35]. The CECT multiphasic protocol should include an abdomen/pelvis pre-contrast scan followed by chest/abdomen/pelvis dynamic images acquired in the arterial and portal venous phases without oral contrast medium (CM). CM volume should be calculated according to patient size based on total body weight (BW), injecting about 0.625 gI per kilogram of total BW. High concentrations (370–400 mg I/mL) of IV CM (80–120 mL of iodinated CM, depending on the patient’s weight) should be administered through an 18–20-gauge needle into the antecubital vein at a rate of 3.5–4 mL/s. This should be followed by a bolus of 30–40 mL of saline at the same flow rate. The acquisition of the arterial phase is timed using bolus tracking, placing the region of interest (ROI) on the aortic arch and starting at an attenuation threshold of 100 Hounsfield Units (HU) [34][35][36][37]. The portal venous phase is acquired with a delay of 60–70 s. The suggested acquisition includes scanning the abdomen and pelvis in the arterial phase, and the chest, abdomen, and pelvis in the portal venous phase. Additionally, a late scan of the abdomen and pelvis at 3–5 min may be acquired to address various causes of shock. Oral or rectal CM is not recommended. Each institution should regularly assess image quality, review protocols regarding dose, and consider the possibility of reducing the quantity of CM [34]. The development of new technologies aims to reduce radiation exposure while maintaining good image quality through iterative reconstruction or automatic tube current modulation [35]. Another option to reduce the radiation dose is the adoption of dual-energy CT, allowing the possibility of virtual noncontrast (VNC) image acquisition [38]. An unenhanced CT brain should be considered for patients presenting with altered mental status, to exclude the presence of acute ischemic stroke or intracranial hemorrhage. Head CT can also be conducted during the late phase of a total body study to rule out the presence of intracranial abscess formation or malignancy [35]. To ensure proper analysis and post-processing, it is recommended to use an effective slice thickness of 2.5 mm with reconstruction at 0.625 mm, allowing for maximum intensity projection (MIP) and multiplanar reformation (MPR) techniques.

3. CT Patterns

CECT images may be used to assess three possible hemodynamic instabilities in acutely sick patients:
(a)
In cases of hemodynamic stability, IV CM into an upper limb vein is delivered to the right atrium via the superior vena cava (SVC), and is then pumped via the right ventricle to the pulmonary arteries. Contrast subsequently returns via the pulmonary veins to the left-side cardiac chambers before reaching systemic circulation [39]. As it undergoes first pass circulation and re-circulation, the contrast bolus gradually mixes with the blood pool, leading to dilution while moving downstream from the injection site. Due to its small molecular size, iodinated CM exhibits high diffusibility, readily redistributing from the intravascular space to organic interstitial spaces [39][40]. This may be called the “physiological” pattern and can correspond to an early compensatory stage of shock. Particularly in these patients without advanced shock symptoms, an image-based morphological indicator promises information about the identification of patients “at high risk”.
(b)
In a state of advanced hemodynamic instability, many homeostatic mechanisms try to maintain arterial pressure and adequate tissue perfusion to critical organs, such as the brain and heart, by reflex stimulation of the sympathetic nervous system, elevated levels of angiotensin II, adrenaline, and noradrenaline, and vasoconstriction (compensated shock). Carotid baroreceptors respond to decreased blood pressure by triggering increased sympathetic signaling and maintaining cardiac output (sympathetic “fight or flight” response). In cases of decompensated shock, when compensatory mechanisms falter and prior to the onset of death, the pumping action of the heart ceases, leading to a substantial decline in systemic arterial and venous pressures. Consequently, the arteriovenous pressure gradient diminishes [6][41][42]. This altered hemodynamic state results in stasis of CM in the venous system in the presence of the left chamber and arterial opacification, and of other infrequent and often unappreciated ominous MDCT vascular signs that represent a true hypovolemic state and must be recognized early by the radiological staff to improve survival [24][43][44][45][46][47][48]. This may be called the “venous CM pooling and layering” pattern, indicating that compensatory mechanisms are becoming insufficient and the patient must receive immediate treatment.
(c)
In irreversible end-organ dysfunction, injected IV CM circulation is supported only by the pressure applied by the automated power injector and the density of contrast material. Circulatory arrest leads to dense contrast pooling and layering in the SVC, IVC (inferior vena cava), and right heart chambers with non-opacified left heart chambers or arterial vessels (Figure 1) [43][45][49][50][51][52]. This may be called the “non-beating heart” pattern. Cardio-pulmonary aggressive resuscitation must immediately be initiated within the framework of a predetermined emergency plan.
Diagnostics 13 02304 g001 550

Figure 1. Non-beating heart in a 72-year-old man with sudden-onset severe dyspnea/shock and asystole during thoraco-abdominal CT. (A) CECT axial image shows dense contrast in the round superior vena cava, and reflux in the azygous arch; (B) contrast pooling and layering in the right atrium and IVC with retrograde opacification of coronary sinus (arrow). (C) CM fills the round inferior vena cava with hypostatic reflux into the hepatic veins, hemiazygos vein, partially splenic vein, and (D) right renal vein. Note no mixing of blood with CM and no opacification of the pulmonary arteries, aorta, and left cardiac chambers, suggestive of a non-beating heart. Prompt initiation of cardio-pulmonary resuscitation to restore circulation was useless. Autopsy: ruptured myocardial infarction.

4. CT-Updated HSC Findings as Diagnostic Biomarkers

CECT shock-associated findings partially overlap with those referred to previously in the literature as CT “hypoperfusion or hypovolemic shock complex” (HSC) [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32]. This refers to a constellation of findings that reflect hypovolemia and is often described in traumatic hemorrhagic shock [15][16][18][21][24][25][26][27][29]. HSC findings can be grouped into vascular (morphological and functional) and, based on their various anatomic locations, visceral/solid organ findings. It is now clear that vascular signs represent the true hypovolemic state and visceral findings represent hypoperfusion [30].

5. CECT Findings/Biomarkers as Prognostic Indicators

The clinical diagnosis of hypovolemic shock is not always obvious in an acute setting due to hemodynamic compensatory mechanisms. Most of the published literature refers to hypovolemic shock, and cardiogenic shock to a lesser extent, often in a trauma setting. There is a scarcity of radiological literature regarding CT findings in distributive and obstructive shock. CT findings are biomarkers that can be used to predict the diagnosis and prognosis of shock as well as being useful for monitoring the response to treatment. While specific CT signs in different subtypes of shock depend on the underlying etiology(ies), CT features generally overlap all forms. To confirm the diagnosis of CT shock syndrome, the presence of two or more vascular, visceral, or parenchymal signs is required [18][27]. The incidence of CT findings as prognostic indicators in various shock types is summarized in Table 2.
Table 2. Incidence and prognostic meaning of CECT findings in each shock type (from references [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96][97][98][99][100][101][102][103][104][105][106]). The presence of two or more vascular, visceral, or parenchymal signs is deemed necessary to establish the presence of CT shock syndrome. IVC, Inferior vena cava; NA, not available; SMA/V, Superior mesenteric artery/vein; AV, Atrio-ventricular.

CECT Findings

Cardiogenic

Distributive

Hypovolemic

Obstructive

Outcome

Small-caliber aorta

~25%

~28%

~30%

~35%

poor

Slit/flattened cava

~70%

~55%

~77%

~50%

very poor

Halo sign IVC

~70%

~65%

~75%

NA

poor

Narrow SMA/V

NA

NA

NA

NA

NA

Lack of left AV enhancement

~65%

~35%

~55%

~20–50%

very poor

CM vascular layering

~75%

NA

~65%

~70%

very poor

Hot-spot sign

NA

NA

NA

NA

NA

Periportal halo

~60%

NA

~40%

NA

NA

Ongoing hemorrhage

10%

15%

65%

25%

poor

Shock Thyroid

NA

NA

NA

NA

very poor

Shock Lungs

NA

NA

NA

NA

NA

Shock Bowel

~55%

~50%

~70%

~40%

poor

Shock Spleen

~40%

~50%

~50%

~25%

poor

Liver altered density

~85%

~55%

~57%

~45%

poor

Shock gallbladder

20–30%

~12%

13–35%

~9%

poor

Shock pancreas

~35%

~55%

~45%

~35%

very poor

Shock Stomach

NA

NA

NA

NA

NA

Shock Kidneys

~55%

~50%

~60%

~40%

poor

Shock Adrenals

~60%

~65%

~55%

~50%

poor

This entry is adapted from the peer-reviewed paper 10.3390/diagnostics13132304

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