JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
RADIOLOGICAL DIAGNOSIS: Hypovolemic shock complex secondary to massive intra-abdominal bleeding
more localized. 5
The kidneys show hyper-enhancement in shock bowel because as angiotensin II is released, glomerular efferent arteriole constriction and increased glomerular filtration results, leading to more contrast in the kidneys and ureters. 4 However, renal hyper-enhancement is a non-specific finding in hypovolemic shock complex. Changes in the pancreas, spleen, and liver can occur, although these findings were not observed in this patient. Extra- peritoneal fluid surrounding the pancreas has been described in HSC in the absence of pancreatic injury due to arteriolar and venous constriction facilitating fluid stasis and subsequent movement of this fluid into the extravascular space. 2 Splenic hypo-enhancement may be seen in HSC as compensatory mechanisms try to shunt blood flow away from the spleen.6 Liver hypo-enhancement is less common due to its dual blood supply and the portal system being less sensitive to epinephrine and norepinephrine. 4 Intense adrenal enhancement, as observed in this patient, may occur due to the fact that this organ is actively releasing epinephrine and norepinephrine, a crucial part of the compensatory mechanisms in hypovolemic shock. 7 Although HSC is well-known in trauma patients, similar CT findings can be found in non-trauma patients also with hypotension. However, a collapsed inferior vena cava (<9 mm diameter at three different levels), is a finding more common in trauma patients. 5 The patient in this case, a non-trauma patient, had a nearly collapsed inferior vena cava. The “halo sign” describes edema surrounding a collapsed IVC and is a finding not specific to HSC alone. 2 Pre-existing atherosclerosis, damage of the mesenteric vessels, or atrial fibrillation can exacerbate the loss of blood flow to splanchnic circulation. The patient had post-operative atrial fibrillation, a known risk factor for non-occlusive mesenteric ischemia that could have exacerbated loss of splanchnic blood flow. 8 Due to her dropping blood pressures, the patient was also administered maximal doses of dopamine, epinephrine, and norepinephrine. The latter two vasopressor agents act directly on alpha-1 adrenergic receptors that control mesenteric vasoconstriction and could have accelerated the presentation of shock bowel by causing nearly immediate mesenteric vessel vasoconstriction. 9 Compared to different forms of acute mesenteric ischemia, treatment for shock bowel is non-surgical and typically involves aggressive fluid resuscitation.
CASE REPORT
70-year-old female inpatient with past medical history of lupus, skin cancer, hypertension, chronic obsctructive pulmonary disease (COPD), cervical cancer, and asthma presented with abdominal pain and hypotension seven days postop. Her self- reported surgical history was significant for three prior bowel surgeries due to perforations. With systolic pressures falling into the 70s, the patient was placed on dopamine, norepinephrine and epinephrine while being transferred to the medical intensive care unit (ICU). CTA of the abdomen/pelvis was ordered for worsening abdominal pain and deteriorating conditions. The exam revealed a right-sided abdominal hematoma and multiorgan hypoperfusion. The patient became obtunded (Glascow Coma Scale score of 3) and expired the following day.
DISCUSSION
Hypovolemic shock complex (HSC), also known as shock bowel, is a subset of non- occlusive mesenteric ischemia that most often is seen in trauma patients with subsequent hemorrhage and hypotension. Non-occlusive mesenteric ischemia (NOMI) accounts for approximately 20% of cases of acute mesenteric ischemia 1 and HSC occurs in approximately 5% of trauma patients. 2 Shock bowel has mortality rates reported between 70 and 90%. 3 Although this patient was not a trauma patient, she had previous surgery and was found to have a large actively bleeding hematoma which resulted in significant volume loss and worsening hypotension. With blood loss/volume loss, a compensatory sympathetic response would occur, releasing angiotensin II, epinephrine, and norepinephrine. Blood flow initially gets shunted away from the splanchnic vasculature to more vital organs, but as hypotension and shock continue to progress, eventually there is loss of this compensation mechanism. 4 Multi-detector computed tomography (CT) has a sensitivity of 64-93% and a specificity of 92-100% in diagnosing bowel ischemia. 1 Shock bowel has multiple classic computed tomography findings. Some can be explained by the pathophysiology occurring, while others have unidentified mechanisms. Furthermore, some of the findings in shock bowel syndrome are not necessarily specific for the syndrome itself. Typically, shock bowl has diffuse small bowel involvement, with little involvement of the colon. 2 Common CT findings include mucosal hyper-enhancement and fluid-filled loops of bowel. During sympathetic compensation, there is arterial vasospasm and venous vasoconstriction in the splanchnic vasculature due to the effects of angiotensin II, epinephrine and norepinephrine. 4 As the intestinal wall mucosa is subjected to ischemia, there is increased permeability, loss of fluid resorption, and loss of peristalsis. 4 These factors result in fluid-filled bowel loops and increased IV contrast in the mucosa of the bowel. These CT findings are typically diffuse, helping to differentiate it from other forms of acute mesenteric ischemia that may be
32 J La State Med Soc VOL 170 JANUARY/FEBRUARY 2018
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