Abstract】A 70-year-old woman was admitted to the hospital with “right hip fracture, weakness and atrial fibrillation with rapid ventricular rate” and was discharged to a community hospital. Two days after discharge, the patient returned to the emergency room with “acute urinary retention and recurrent rapid heart rate”. In addition to the chief complaint, the patient complained of generalized weakness and median lower abdominal pain. He denied any previous history of urinary retention and had no history of fever, dysuria, hematuria, vomiting, dyspnea, or chest pain. Past history: hemiparesis of the left limb due to stroke, history of hypertension, atrial fibrillation, epilepsy, knee meniscus replacement, and usually bedridden. Usual treatment medications were atorvastatin, enoxaparin, levetiracetam (antiepileptic drug), metoprolol, omeprazole and warfarin (7.5 mg once daily).
On examination, the patient was nervous because of pain, had low blood pressure, BP 73/45 mm Hg, rapid heart rate, about 180 bpm, and no fever (T 36.6°C). Oxygen saturation (SO2) was 97% (2 L/min of oxygen). Head, neck and lung examination was unremarkable. The heart rate was fast, the heart sounds on auscultation were variable in intensity, and there was no jugular venous anger or bilateral lower limb edema. The abdominal skin was left with a needle eye due to subcutaneous enoxaparin injection, abdominal muscle tension, diffuse tenderness throughout the abdomen, no rebound pain, and diminished bowel sounds on auscultation. Neurological examination suggested hemiparesis of the left limb, and the rest of the examination was not special.
Ancillary tests: complete blood count and emergency metabolic tests (including liver function, renal function, blood glucose and electrolytes) suggested leukocytosis, WBC 28.1×109/L, anemia, HB 7.3 gm/dL, HCT 21.1%, elevated potassium 5.9 mmol/L, renal insufficiency, creatinine (Cr) 1.6 mg/dL, urea nitrogen (BUN) 32 mg/ dL, estimated glomerular clearance (eGFR) of 32, increased anion gap, (AP=23 mEq/L) and acidosis with increased anion gap (HCO3- of 15 mmol/L). Liver enzymes were elevated: alkaline phosphatase (AP) 126 IU/L, ALT 73 IU/L, AST 129 IU/L. Prothrombin time (PT) was prolonged at 18.2 and international normalized ratio (INR) of prothrombin time was 1.62. creatine phosphokinase (CK) 21 IU/L, CK-MB isoenzyme 1.8 ng/mL, troponin (TnT) The electrocardiogram showed atrial fibrillation with rapid ventricular rate, but no evidence of significant myocardial ischemia. The chest radiograph did not suggest a significant acute lesion. A combined abdominal and pelvic CT scan suggested a 15 cm x 13 cm hypodense mass behind the left rectus abdominis muscle with some hyperdense shadowing (Figure 1) and collapsed inferior vena cava (Figure 2).
Figure 1
Figure 1 shows a large hematoma attached to the wall and a 15 x 13 cm hypodense mass with high density shadow on CT.
Figure 2
Figure 2 shows the collapsed inferior vena cava.
After a rapid infusion of 500 ml of saline, the heart rate and blood pressure improved slightly, and it was decided to continue drug therapy to control the ventricular rate of atrial fibrillation without electrical diversion. At the same time, a urinary catheter was placed in the patient, but no urine was exported. The blood pressure did not return to normal, but the heart rate slowed down to 129 beats/min, and diltiazem was given intravenously to control the ventricular rate of atrial fibrillation. After 24 hours of aggressive resuscitation treatment, a total of 4250 ml of saline was supplemented, 3 units of blood (600 ml of pressurized red) and 4 units of fresh frozen plasma (800 ml) were transfused. Despite aggressive fluid resuscitation, blood pressure continued to be difficult to restore, and treatment with intravenous norepinephrine to raise blood pressure was started. The patient’s abdomen was significantly tense and painful, and intra-abdominal pressure (IAP) was measured at 24 mm Hg. A surgical consultation was immediately obtained and the patient was asked to continue supportive therapy. 38 mm Hg was retested 6 hours later.
The patient’s diagnosis?
Abdominal septal compartment syndrome
Hint: The normal value of intra-abdominal pressure is 0-5 mm Hg.
The main features of this patient are refractory hypotension, oliguria, metabolic acidosis and anemia. ct shows abdominal wall hematoma and collapsed inferior vena cava. Intravesical pressure was measured to be elevated and continued to be elevated during emergency observation. The clinical diagnosis of abdominal compartment syndrome (ACS) was made on the basis of multiple organ failure, abdominal wall hematoma due to anticoagulants, and elevated intra-abdominal pressure.
Septal compartment syndrome (CS) is an increase in pressure in a fixed compartment of the body due to trauma or other causes, resulting in decreased blood flow in the microcirculation, tissue ischemia, and organ insufficiency. The typical clinical manifestations are “6Ps”, i.e. pain, pressure, paresthesias, skin temperature changes (poikilothermia), and paralysis. The first three symptoms appear earlier. The first three symptoms appear early and the last three are late manifestations. Abdominal pain and increased abdominal pressure may be early signs of abdominal septal compartment syndrome, while multiple organ failure and hypotension of the body circulation are late signs.
The abdominal septal compartment syndrome is the result of an adverse physiological response to an acute increase in intra-abdominal pressure (IAP). Intra-abdominal hypertension (IAH) is defined by the World Federation of Abdominal Septal Chamber Syndrome as an increase in intra-abdominal pressure of ≥12 mm Hg. A sustained increase in intra-abdominal pressure of ≥20 mm Hg may trigger organ insufficiency or failure. Cavernous organ insufficiency can also be the result of direct pressure. Elevated abdominal pressure causes collapse of tissue structures, thrombosis, or edema of the intestinal wall, resulting in bacterial ectopic and fluid accumulation that further increases intra-abdominal pressure. Impaired oxygen delivery at the cellular level causes tissue ischemia and hypoxic metabolism, increased secretion of vasoactive substances such as histamine and ano-hydroxytryptamine, and increased permeability of the endothelium. Impaired capillary permeability causes impaired oxygen transport and delivery by red blood cells.
The abdominal septal compartment syndrome is divided into primary, secondary and chronic forms. Those directly caused by intra-abdominal organ lesions are called primary or acute abdominal septal compartment syndrome. For example, penetrating abdominal injuries, intraperitoneal hemorrhage, pancreatitis, pelvic fracture ruptured abdominal aortic aneurysm, etc. Secondary abdominal septal compartment syndrome has no visible intra-abdominal organ damage, but extra-abdominal injuries can cause fluid accumulation, including massive fluid resuscitation (>3 L), massive deep burns, post-surgical procedures, and sepsis. Chronic abdominal septal compartment syndrome can also be caused by massive ascites in cirrhosis.
There are many risk factors for acute celiac septal compartment syndrome, including post-surgical procedures, major trauma or burns, central obesity with high BMI (body mass index) and reduced abdominal wall compliance in mechanically ventilated patients, increased intestinal contents due to gastroparesis, intestinal obstruction, colonic pseudo-obstruction, or intra-abdominal or retroperitoneal tumors; increased abdominal contents due to pneumoperitoneum, pneumoperitoneum, or ascites; in acidosis and hypotension increased capillary permeability and fluid accumulation; hypothermia; massive blood transfusion (more than 10 U in 24 hours); massive fluid resuscitation (more than 5 L in 24 hours); pancreatitis sepsis, etc. Enoxaparin-induced retroperitoneal hemorrhage and acute abdominal septal compartment syndrome have also been reported clinically.
Acute abdominal septal compartment syndrome should be considered in patients presenting with 2 or more risk factors or progressive organ insufficiency, and relevant investigations should be performed. Examination for acute abdominal septal compartment syndrome includes serial abdominal plain films to look for free gas or intestinal obstruction. Abdominal CT may show a “rounded abdomen” (dilated abdomen with an increased ratio of anterior to posterior diameter to transverse diameter >0.80), collapsed vena cava, or thickened bowel wall. Intra-abdominal pressure should also be measured. Measurement of intra-abdominal pressure can be determined by insertion of a Foley catheter. The change in intra-abdominal pressure is reflected by measuring the change in intra-vesical pressure, which is parallel to the change in intra-abdominal pressure. The normal values of intra-abdominal pressure vary with the patient: 0-5 mm Hg in healthy adults, 5-7 mm Hg in critically ill patients, 10-15 mm Hg in open patients, 15-25 mm Hg in patients in septic shock, and 25-40 mm Hg in patients with acute abdomen.Burch and colleagues classified the intra-abdominal pressure measured by the intra-vesical catheter according to the A recent multicenter prospective epidemiologic study reported that the mean intra-abdominal pressure in patients admitted to the ICU was 10 ± 4.8 mm Hg, with 67.9% of patients having intra-abdominal pressures within the normal range (<12 mm Hg) and 32.9% of patients having intra-abdominal pressures within the normal range (<12 mm Hg). 12 mm Hg), 32.1% of patients had intra-abdominal hypertension (IAH >12 mm Hg), and 4.2% had acute abdominal septal compartment syndrome. The incidence of acute abdominal septal compartment syndrome in patients with intra-abdominal hypertension was 12.9%. Mortality was significantly higher in the intra-abdominal hypertension group compared to the non-IAH group.
The hemodynamic effects of intra-abdominal hypertension (IAH) are a decrease in cardiac output and a decrease in volume per beat, leading to a decrease in intra-abdominal superior mesenteric and renal artery flow, an increase in oxygen consumption, and a decrease in arterial partial pressure of oxygen and pH. Possible explanations for the decreased cardiac output are compression of the inferior vena cava, resulting in a decrease in venous return blood volume. In addition, an increase in afterload may also account for the hypotension in the body circulation. Increased intra-abdominal pressure results in restricted diaphragmatic inferior displacement, resulting in decreased lung and chest wall compliance, thus affecting pulmonary respiratory function. In addition, mechanical ventilation may also increase intra-abdominal pressure. Intra-abdominal hypertension (IAH) also decreases renal blood flow and reduces glomerular filtration rate. The case physiological mechanisms underlying intra-abdominal hypertension (IAH) are not well understood, but are not exclusively the result of reduced cardiac output. Shunting from the renal cortex to the medulla also reduces renal blood flow, and high levels of antidiuretic hormone secretion may also contribute to renal dysfunction. The severity of abdominal blood flow disorders is usually evaluated using the abdominal perfusion pressure (APP), which is calculated as the mean arterial pressure minus the IAP, and the APP should be maintained above 50-60 mm Hg. APP is superior to IAP, arterial pH, base residual and arterial lactate values in predicting organ insufficiency and patient outcome.
The treatment of abdominal septal compartment syndrome (ACS) includes several aspects, depending mainly on the severity of the patient’s condition and the underlying etiology. Because of the many etiologies of IAH/ACS, there is no uniform treatment strategy. proper treatment of IAH/ACS is based on three main principles: serial monitoring of IAP, maintenance of good perfusion of the body circulation and support of organ function, and refractory intra-abdominal hypertension (IAH) requiring immediate surgical decompression. Most patients with grade III and all patients with grade IV elevated intra-abdominal pressure require surgical decompression therapy. Conservative treatment is appropriate for grade I and grade II patients with primary flares. Treatment includes position change, gastrointestinal decompression and anal vent decompression, fluid resuscitation, diuretic and renal replacement therapy, and percutaneous catheter decompression.
In this case, after correction of warfarin-induced coagulation disorder with fresh plasma and vitamin K supplementation, the patient was taken to the operating room for resection of the abdominal wall hematoma. No active bleeding was detected intraoperatively, and the wound was plugged with hemostatic material and the abdominal cavity was kept open to reduce the IAP. after the patient’s condition improved significantly the next day, the patient was re-admitted to the operating room to remove the plug and close the abdominal cavity. Apart from some blood clots, no active arterial or venous bleeding was detected, and an abdominal drainage tube was placed for negative pressure drainage. Subsequently, the patient’s clinical symptoms improved and multiorgan failure resolved, and he was finally transferred to a general ward, where the drainage tube was removed and he was discharged.
Quiz.
Which of the following 4 patients has the greatest possible risk of developing intra-abdominal hypertension (IAH) or abdominal septal compartment syndrome (ACS)? (D)
A. 28-year-old patient with acute appendicitis
B. 72-year-old patient with asymptomatic abdominal aortic aneurysm
C. 66-year-old patient with acute exacerbation of chronic obstructive pulmonary disease
D．A 58-year-old male patient with cirrhotic ascites
Answer Explanation.
Screening for abdominal compartment syndrome (ACS) should be performed in patients with 2 or more risk factors or new or progressive organ failure. There are many risk factors for acute abdominal compartment syndrome, including decreased abdominal wall compliance in patients with post-surgical procedures, major trauma or burns, central obesity with high BMI (body mass index) and mechanical ventilation, increased intestinal contents due to gastroparesis, intestinal obstruction, colonic pseudo-obstruction, or intra-abdominal or retroperitoneal tumors; increased abdominal contents due to pneumoperitoneum, pneumoperitoneum, or ascites; acidosis and hypotension in increased capillary permeability and fluid accumulation; hypothermia; massive blood transfusion (more than 10 U in 24 hours); massive fluid resuscitation (greater than 5 L in 24 hours); pancreatitis sepsis, etc. Large amounts of ascites in cirrhosis can also cause chronic abdominal septal compartment syndrome.
How would you monitor a patient if you suspect intra-abdominal hypertension (IAH) or abdominal compartment syndrome (ACS)?C
A. central venous pressure
B. Serial renal, ureteral, and bladder x-rays
C. Bladder pressure monitoring
D．Series arterial blood gas and lactate monitoring
Intra-vesical pressure can be monitored by insertion of a Foley catheter, with changes in intra-abdominal pressure paralleling changes in intra-vesical pressure.
Main abbreviations.
ACS Abdominal compartment syndrome
APP Abdominal perfusion pressure
CS Compartment syndrome 中隔室 syndrome
IAP Intra-abdominal pressure
IAH Intra-abdominal hypertension