case presentation
A 53-year-old female patient with a history of liver cirrhosis due to alcoholism presented to the emergency department with diffuse abdominal pain and fatigue that persisted for 2 days. The pain was sudden. In the past two days, the patient’s diet decreased, no fever, vomiting, no abnormal bowel movements, no blood in the stool or black stools. The patient had never undergone surgery and had experienced 1 normal delivery.
(1) Vital signs: blood pressure 82/57 mmHg; heart rate 96 beats/min; body temperature 37.3℃; respiratory rate 16 beats/min; Oxygen inhalation 2L/min, blood oxygen saturation was 92%. Drowsiness, scleral jaundice. Cardiopulmonary function tests were normal. The abdomen was palpated for increased tone, swelling, and diffuse pain. pitting edema of both lower extremities (degree +2). Flapping wing tremors. MELD score is 18.
(2) Laboratory tests: hemoglobin 9.8g/dL (reference range 11.5-15.5); platelet count 100×10^9/L (150–400); white blood cell count 9.9×10^9/L (3.7-11.0); serum creatinine 1.06 mg/dL (0.58-0.96); bilirubin 6.3 mg/dL (0.2-1.3); prothrombin time The international normalized ratio (INR) of 2.15 (0.8-1.2); blood urea nitrogen 13 mg/dL (7-21); serum albumin 2.7 g/dL (3.9-4.9).
Intravenous fluid resuscitation was initiated, but the patient remained hypotensive and repeated laboratory tests 4 hours later, his hemoglobin level dropped to 7.3 mg/dL.
Differential Diagnosis
Question: Which of the following may be The cause of this patient’s clinical presentation?
(1) spontaneous bacterial peritonitis
(2) esophageal variceal bleeding
< p>(3) Portal vein thrombosis
(4) Rupture of abdominal aortic aneurysm
(5) Rupture of splenic aneurysm
01
Spontaneous bacterial peritonitis
10%-20% of cirrhosis Spontaneous peritonitis occurs in hospitalized patients with ascites. Patients may present with ascites and abdominal pain, tenderness, fever, encephalopathy, or worsening liver and kidney function.
Diagnostic paracentesis is more valuable than other tests in identifying the cause of ascites. Physicians should calculate serum-ascites albumin gradients and perform cell counts and ascites cultures. Spontaneous peritonitis can be diagnosed if the neutrophil count in ascites is ≥0.25 × 10^9/L, even if the culture of ascites is negative. Blood cultures should also be performed because 50% of patients will have bacteremia.
5% of cases of infectious ascites are secondary bacterial peritonitis caused by organ perforation or intra-abdominal abscess, which is difficult to differentiate from spontaneous peritonitis clinically, but CT can be used for differential diagnosis. This patient may present with septic shock secondary to any of the above causes.
02
Esophageal variceal bleeding
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Half of the patients with liver cirrhosis had esophagogastric varices, which were mainly caused by portal hypertension. Patients require gastroscopy, and rapid fluid resuscitation, diagnosis, and control of bleeding are paramount.
Esophagus, stomach, and duodenal endoscopy can be used for diagnosis and treatment. Short-term prophylactic antibiotics can prolong survival by preventing infection in the bleeding area. This patient may present with hemorrhagic shock from esophageal variceal bleeding.
03
Portal vein thrombosis
Portal vein thrombosis is a common complication of liver cirrhosis, with an incidence of 5% to 28%. Risk increases with the severity of liver disease and is associated with hepatocellular carcinoma. 43% of cases were detected incidentally on ultrasonography in asymptomatic patients, 39% presented with upper gastrointestinal bleeding, and 18% presented with abdominal pain.
Portal vein thrombosis is the blockage of all or part of the blood flow of the portal vein caused by the blockage of the thrombus in the portal vein lumen. Ultrasonography and CT can be used to confirm the diagnosis.
This patient’s thrombocytopenia reflects the severity of portal hypertension and increases the risk of portal vein thrombosis, but this is unlikely to be the cause of this patient’s hemodynamic The only reason for learning to change.
04
Ruptured abdominal aortic aneurysm
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Ruptured abdominal aortic aneurysm is an emergency with a mortality rate approaching 90%. Risk factors for abdominal aortic aneurysm are smoking, male sex, age over 65 years, history of cardiovascular disease, hypertension, and family history of abdominal aortic aneurysm (especially if first-degree relatives are affected).
Compared with open surgery, endovascular interventional repair has lower mortality and complication rates. The patient did not have any of these risk factors, so this diagnosis is unlikely.
05
ruptured splenic aneurysm
Splenic aneurysm is the third most common intra-abdominal aneurysm, after abdominal aortic aneurysm and iliac aneurysm. The disease is usually asymptomatic, and detection rates are higher with increased use of CT. Symptomatic splenic aneurysms present with abdominal pain and potential rupture, which is often life-threatening.
Considering the presence of hypovolemic shock, this patient may have ruptured a splenic aneurysm.
Case Tracking: Ruptured Splenic Aneurysm
Emergency Contrast-Enhanced CT of the Abdomen and Pelvis A large left intra-abdominal hematoma is shown, bleeding continuously from a ruptured splenic aneurysm. The patient was transfused with packed red blood cells and fresh frozen plasma before being transferred to the hospital.
Overview of splenic aneurysms
Splenic aneurysms are the most common visceral aneurysms. True aneurysms involve three layers of the arterial wall, the intima, media, and adventitia. Liver cirrhosis and portal hypertension are associated with true aneurysm formation. The mechanism of splenic aneurysm formation may be the increase in splenic blood flow caused by portal vein congestion, resulting in changes in hemodynamic pressure, damage to the structure of the arterial wall, and resulting in expansion of the aneurysm. Portal hypertension after liver cirrhosis is one of the high-risk factors for splenic aneurysm.
The onset of splenic aneurysm is insidious, and most of them have no obvious symptoms before rupture, with occasional left upper quadrant discomfort. Once obvious symptoms such as left upper quadrant pain, nausea, and vomiting appear, it often indicates that the aneurysm ruptures. After rupture, there are symptoms such as severe upper abdominal pain, hypotension, and shock. In some splenic aneurysms, rupture and bleeding are the first symptoms, and shock and even death occur soon.
In earlier reports, the incidence of true splenic aneurysm in patients with portal hypertension was 2.9%-50%, the latter being the splenic hilum at autopsy in patients with liver cirrhosis. Incidence of small and medium aneurysms. The incidence of clinically apparent aneurysms in patients with cirrhosis is currently unknown, but asymptomatic splenic aneurysms are increasingly found in imaging screening studies.
The risk of rupture of a splenic aneurysm is very low, only 2%-10% in elderly patients, and with the increase in asymptomatic splenic aneurysms detected by incidental examination, splenic The risk of aneurysm rupture may be even lower. However, emergency treatment of ruptured splenic aneurysms is paramount in tertiary care because the mortality rate for ruptured splenic aneurysms ranges from 29% to 36%.
Splenic artery pseudoaneurysms are rare, and their pathophysiological processes are different from true aneurysms. It usually occurs in trauma, pancreatitis, or after surgery. Pseudosplenic aneurysms are more prone to rupture due to disruption of the integrity of the vessel wall. Therefore, regardless of the size of the pseudoaneurysm, treatment is required.
Risk factors for splenic aneurysms
Risk factors for true aneurysms include hypertension , atherosclerosis, portal hypertension with or without cirrhosis, liver transplantation, late pregnancy, and multiple pregnancy. Splenic aneurysms are usually diagnosed in 50-60 years of age. Due to hormonal influence, women may be 4 times more likely to develop the disease than men. Cirrhosis is also associated with large splenic aneurysms (≥5 cm). Although very rare, giant splenic aneurysms are more common in men (male to female ratio 1.78:1) and have a higher risk of rupture. The incidence of splenic aneurysm rupture increases by 3% to 4% after liver transplantation. Rare causes of true aneurysms include fibrodysplasia, collagen vascular disease, vasculitis, and bacterial aneurysms.
The patient’s age and history of cirrhosis put her at increased risk of developing a splenic aneurysm. The risk of rupture is highest in patients with cirrhosis during perinatal and pregnancy.
Treatment of splenic aneurysms
Complications of splenic aneurysms depend on the aneurysm type and causative factors.
Treatment indications for true aneurysm include:
(1) Clinical symptoms caused by aneurysm;
(2) ) diameter ≥2cm;
(3) Surgical procedures such as portal vein shunt surgery and liver transplantation are required;
(4) Women of childbearing age who plan to become pregnant.
The late mortality rate of conservative treatment was 4.9%. Interventional treatments include percutaneous aneurysm embolization or stenting, or open surgery for ligation or resection of the splenic artery.
Both endovascular interventional procedures and open surgical repair have been used for the treatment of splenic aneurysms. The method used depends on the patient’s surgical history, aneurysm anatomy such as splenic artery tortuosity obstructing the passage of the catheter. Compared with interventional surgery, open surgery is associated with longer duration, longer hospital stay, higher 30-day mortality, and higher perioperative complication rates. The complication rate of aneurysm persistence or recurrence within 30 days after endovascular repair is 3% to 5%; therefore, surgical monitoring is recommended. Endovascular interventional repair has a higher reoperation rate, but it is still more cost-effective than open surgery.
Because of the high risk of surgical complications in patients with liver cirrhosis, elective endovascular intervention may be a feasible option for patients at high risk of aneurysm rupture. Complications of endovascular interventional therapy for visceral aneurysms include post-embolization syndrome (fever, abdominal pain, pleural effusion, pancreatitis), puncture site hematoma, splenic infarction, and persistent abdominal pain.
Patients with splenic aneurysms due to cirrhosis tend to require longer hospitalization after endovascular intervention, but there is insufficient evidence to suggest higher other Complication risk.
Summary
Splenic aneurysm is a common complication of liver cirrhosis, but due to the Occult, usually diagnosed incidentally. Elective aneurysm embolization should be considered for asymptomatic splenic aneurysms larger than 2 cm in diameter, symptomatic aneurysms, women of childbearing age, and patients who are preparing for liver transplantation. Although splenic aneurysm rupture is rare, its high mortality rate requires high vigilance for early professional intervention. It is recommended that splenic aneurysm rupture should be considered in the differential diagnosis of cirrhotic patients presenting with abdominal pain, altered mental status, and hemorrhagic shock.
Yimaitong compiled and compiled from: Houriya Ayoubieh, Eyas Alkhalili. Another complication of cirrhosis. Cleveland Clinic Journal of Medicine. DOI: https://doi.org /10.3949/ccjm.84a.16084