Spontaneous Splenic Rupture and Anisakis Appendicitis
Spontaneous Splenic Rupture and Anisakis Appendicitis
A 53-year-old Caucasian woman was admitted to the emergency department (ED) at our institution because of sudden, severe abdominal pain after eating anchovies, as well as weakness, diaphoresis and hypotension. She rated her pain as 8 on a scale of 0 to 10 (with 10 representing the most severe pain). On examination, she was found to be pale, profusely diaphoretic and in extreme discomfort. At the time of admission, her blood pressure was 84/49 mmHg, her pulse was 110 beats/minute, her respiration was 20 breaths/minute and shallow and her oxygen saturation was 98% while she was breathing ambient air. Her neck was supple, and her chest was clear. Her abdomen was diffusely tender, with guarding in the epigastrium. The point of greatest tenderness was in the periumbilical area. Blood was drawn for laboratory testing, and a peripheral 20-gauge intravenous line was placed. Crystalloid intravenous solution was infused rapidly, and oxygen was administered at a rate of 2 L/minute by nasal cannula.
She had been evaluated several times previously in the ED because of abdominal pain. Her discomfort had begun 6 months earlier and was localized to the epigastrium. At that time, she described a constant pressure unrelated to food intake that was associated with intermittent nausea and vomiting. She reported no change in urine or stools and no hematochezia, melena, dysphagia, anorexia, increase in abdominal girth, early satiety or change in weight in the months before that admission. On examination at that time, her abdomen was slightly distended, her pain was improved, surgical etiologies were ruled out and she was discharged with close follow-up. Her medical history included hyperlipidemia, hypertension, gastroesophageal reflux disease and diabetes mellitus type 2. She had had no previous operations. She did not drink alcohol or use illicit drugs. She smoked cigarettes (20 pack-years). Her medications on admission included fluvastatin (80 mg daily), lansoprazol (15 mg daily), irbesartan (300 mg daily), metformin (850 mg twice daily) and acetylsalicylic acid (100 mg daily). The patient had had high serum-specific immunoglobulin E (IgE) (25 kU/L) against A. simplex in a previous analysis 4 months earlier. A previous upper endoscopy had revealed mild to moderate gastric edema of the greater curvature.
The patient had eaten anchovies 48 hours before the onset of symptoms, despite having been warned not to do so. Approximately 30 minutes after her admission to the ED and 60 minutes after the onset of symptoms, her blood pressure was 65/35 mmHg and her pulse was 118 beats/minute. She appeared to be in severe distress. Her abdomen was diffusely tender without abdominal ecchymosis or palpable masses. Distal pulses were present. Laboratory studies revealed that her white blood cell count was 13,160 cells/μl with predominant eosinophilia, hemoglobin concentration was 7.9 g/dl, serum C-reactive protein was > 67 U/L, D-dimer was 550 ng/mm, hematocrit was 22.4% with a mean corpuscular volume of 87.9 fl, platelet count was 301,000/mm, sodium level was 138 mmol/L, potassium was 4.8 mmol/L, bicarbonate was 25 mmol/L, blood urea nitrogen was 44 mg/dl, creatinine was 0.6 mg/dl and glucose was 112 mg/dl. Her alanine aminotransferase level was 27 U/L, aspartate aminotransferase was 35 U/L, alkaline phosphatase was 45 U/L, total bilirubin was 0.5 mg/dl, total protein was 7.4 mg/dl and amylase was 47 U/L. Her international normalized ratio was 0.9. In addition to crystalloid intravenous solution, uncrossed packed red blood cells were transfused simultaneously.
The differential diagnosis of shock in this patient with abdominal pain included hemorrhage, which can result from a perforated viscus, a ruptured abdominal aortic aneurysm or a ruptured ovarian cyst. Processes that cause hypovolemia because of interstitial fluid sequestration, such as pancreatitis, or that cause relative hypovolemia, such as a sepsis syndrome due to bacterial peritonitis, were unlikely to have caused such precipitous decompensation. Cardiogenic causes were also considered.
Contrast-enhanced computed tomographic (CT) scanning of the abdomen revealed a splenic subcapsular hematoma with loss of normal structure and normal density of the lower pole, consistent with acute spontaneous splenic rupture. It was accompanied by perihepatic, pelvic and perisplenic free fluid, compatible with hemoperitoneum (Figures 1 and 2). In the retrocecal region, the appendix showed inflammation and mesenteric fat infiltration. The appendiceal wall was thickened. These findings were suggestive of acute appendicitis (Figures 3 and 4). The diagnosis of anisakiasis was primarily suspected on the basis of common anamnesis (history of specific antibodies against Anisakis antigen in the serum), CT findings of appendicitis and the detection of eosinophilia in the differential blood picture.
(Enlarge Image)
Figure 1.
Contrast-enhanced computed tomographic scan of the abdomen revealing splenic subcapsular hematoma with loss of normal structure and normal density of the lower pole, consistent with acute spontaneous splenic rupture.
(Enlarge Image)
Figure 2.
Contrast-enhanced computed tomographic scout view of the abdomen showing splenic subcapsular hematoma with loss of normal structure and normal density of the lower pole, consistent with acute spontaneous splenic rupture.
(Enlarge Image)
Figure 3.
Contrast-enhanced computed tomographic scan of the abdomen revealing the retrocecal region of the appendix with inflammation and mesenteric fat infiltration and a thickened appendiceal wall, suggesting acute appendicitis.
(Enlarge Image)
Figure 4.
Contrast-enhanced computed tomographic scout view of the abdomen revealing the retrocecal region of the appendix with inflammation and mesenteric fat infiltration and a thickened appendiceal wall, suggesting acute appendicitis.
After consultation with the surgeons, the patient was emergently taken to the operating room. Exploratory laparotomy was performed. After opening the abdomen, 2000 ml of blood were removed immediately. Surgery showed splenic subcapsular rupture and intraperitoneal blood with an otherwise normal spleen. The appendix was also removed, showing an acutely inflamed and non-perforated appendix. The pathology report demonstrated the spleen to be mildly enlarged and the parenchyma to be normal. The rupture was found on the medial side, penetrating into the parenchyma of the spleen. Histopathological analysis of the appendectomy specimen revealed the presence of intense inflammatory infiltrate composed of neutrophils and leukocytes accompanied by abundant eosinophils, suggestive of Anisakis appendicitis (Figures 5 and 6). Upon interrogation approximately 3 weeks later, the patient reported intermittent crampy abdominal pain located in the right lower quadrant that radiated to the right flank and was associated with borborygmi and diarrhea. The diagnosis was confirmed later by the detection of Anisakis Deoxyribonucleic acid (DNA) in the resected appendix on the basis of nested polymerase chain reaction. Paired acute-phase and convalescent sera provided no evidence of acute viral infection, and cultures from blood, sputum, stool and urine were negative. Screening for autoantibodies was negative. The patient's hospital course was uneventful, and she was discharged on postoperative day 5.
(Enlarge Image)
Figure 5.
Microscopic histopathological examination of the appendectomy specimen revealing the presence of intense inflammatory infiltrate composed of neutrophils and leukocytes accompanied by abundant eosinophils, suggestive of Anisakis appendicitis.
(Enlarge Image)
Figure 6.
Microscopic histopathological examination of the appendectomy specimen revealing the presence of intense inflammatory infiltrate composed of neutrophils and leukocytes accompanied by abundant eosinophils, suggestive of Anisakis appendicitis.
The results of serologic testing during the patient's hospital course and after discharge were negative throughout, including tests for antibodies to varicella zoster virus IgG. The results of all the following tests were negative: syphilis; antibodies to Epstein-Barr virus IgG and IgM, cryptococcus, rickettsia and human immunodeficiency virus (HIV); antigens of cytomegalovirus (CMV); and nucleic acids of CMV and HIV. The following test results were normal: direct Coombs antibody test; cold agglutinin screening and testing for lupus anticoagulant; hemoglobin electrophoresis; and levels of fibrinogen, homocysteine, lipoprotein (a), β2-glycoprotein I, anti-thrombin III and protein C (functional). At the time of her current admission her total IgE level was 760 kU/l and her specific IgE against Anisakis simplex was > 100 kU/l. Two months later her IgE level was 221 kU/l, and her specific IgE against Anisakis simplex was 34 kU/l. An upper endoscopy examination was later performed. Macroscopic examination revealed signs of moderate inflammation of the gastric mucosa, and a gastric biopsy revealed small areas of granulation tissue that had evidence of eosinophilic leukocyte infiltration within the gastric muscularis layer. The patient currently remains on active duty at work, and at her 18-month follow-up she reported doing well since being discharged, with no known sequelae.
Case Presentation
A 53-year-old Caucasian woman was admitted to the emergency department (ED) at our institution because of sudden, severe abdominal pain after eating anchovies, as well as weakness, diaphoresis and hypotension. She rated her pain as 8 on a scale of 0 to 10 (with 10 representing the most severe pain). On examination, she was found to be pale, profusely diaphoretic and in extreme discomfort. At the time of admission, her blood pressure was 84/49 mmHg, her pulse was 110 beats/minute, her respiration was 20 breaths/minute and shallow and her oxygen saturation was 98% while she was breathing ambient air. Her neck was supple, and her chest was clear. Her abdomen was diffusely tender, with guarding in the epigastrium. The point of greatest tenderness was in the periumbilical area. Blood was drawn for laboratory testing, and a peripheral 20-gauge intravenous line was placed. Crystalloid intravenous solution was infused rapidly, and oxygen was administered at a rate of 2 L/minute by nasal cannula.
She had been evaluated several times previously in the ED because of abdominal pain. Her discomfort had begun 6 months earlier and was localized to the epigastrium. At that time, she described a constant pressure unrelated to food intake that was associated with intermittent nausea and vomiting. She reported no change in urine or stools and no hematochezia, melena, dysphagia, anorexia, increase in abdominal girth, early satiety or change in weight in the months before that admission. On examination at that time, her abdomen was slightly distended, her pain was improved, surgical etiologies were ruled out and she was discharged with close follow-up. Her medical history included hyperlipidemia, hypertension, gastroesophageal reflux disease and diabetes mellitus type 2. She had had no previous operations. She did not drink alcohol or use illicit drugs. She smoked cigarettes (20 pack-years). Her medications on admission included fluvastatin (80 mg daily), lansoprazol (15 mg daily), irbesartan (300 mg daily), metformin (850 mg twice daily) and acetylsalicylic acid (100 mg daily). The patient had had high serum-specific immunoglobulin E (IgE) (25 kU/L) against A. simplex in a previous analysis 4 months earlier. A previous upper endoscopy had revealed mild to moderate gastric edema of the greater curvature.
The patient had eaten anchovies 48 hours before the onset of symptoms, despite having been warned not to do so. Approximately 30 minutes after her admission to the ED and 60 minutes after the onset of symptoms, her blood pressure was 65/35 mmHg and her pulse was 118 beats/minute. She appeared to be in severe distress. Her abdomen was diffusely tender without abdominal ecchymosis or palpable masses. Distal pulses were present. Laboratory studies revealed that her white blood cell count was 13,160 cells/μl with predominant eosinophilia, hemoglobin concentration was 7.9 g/dl, serum C-reactive protein was > 67 U/L, D-dimer was 550 ng/mm, hematocrit was 22.4% with a mean corpuscular volume of 87.9 fl, platelet count was 301,000/mm, sodium level was 138 mmol/L, potassium was 4.8 mmol/L, bicarbonate was 25 mmol/L, blood urea nitrogen was 44 mg/dl, creatinine was 0.6 mg/dl and glucose was 112 mg/dl. Her alanine aminotransferase level was 27 U/L, aspartate aminotransferase was 35 U/L, alkaline phosphatase was 45 U/L, total bilirubin was 0.5 mg/dl, total protein was 7.4 mg/dl and amylase was 47 U/L. Her international normalized ratio was 0.9. In addition to crystalloid intravenous solution, uncrossed packed red blood cells were transfused simultaneously.
The differential diagnosis of shock in this patient with abdominal pain included hemorrhage, which can result from a perforated viscus, a ruptured abdominal aortic aneurysm or a ruptured ovarian cyst. Processes that cause hypovolemia because of interstitial fluid sequestration, such as pancreatitis, or that cause relative hypovolemia, such as a sepsis syndrome due to bacterial peritonitis, were unlikely to have caused such precipitous decompensation. Cardiogenic causes were also considered.
Contrast-enhanced computed tomographic (CT) scanning of the abdomen revealed a splenic subcapsular hematoma with loss of normal structure and normal density of the lower pole, consistent with acute spontaneous splenic rupture. It was accompanied by perihepatic, pelvic and perisplenic free fluid, compatible with hemoperitoneum (Figures 1 and 2). In the retrocecal region, the appendix showed inflammation and mesenteric fat infiltration. The appendiceal wall was thickened. These findings were suggestive of acute appendicitis (Figures 3 and 4). The diagnosis of anisakiasis was primarily suspected on the basis of common anamnesis (history of specific antibodies against Anisakis antigen in the serum), CT findings of appendicitis and the detection of eosinophilia in the differential blood picture.
(Enlarge Image)
Figure 1.
Contrast-enhanced computed tomographic scan of the abdomen revealing splenic subcapsular hematoma with loss of normal structure and normal density of the lower pole, consistent with acute spontaneous splenic rupture.
(Enlarge Image)
Figure 2.
Contrast-enhanced computed tomographic scout view of the abdomen showing splenic subcapsular hematoma with loss of normal structure and normal density of the lower pole, consistent with acute spontaneous splenic rupture.
(Enlarge Image)
Figure 3.
Contrast-enhanced computed tomographic scan of the abdomen revealing the retrocecal region of the appendix with inflammation and mesenteric fat infiltration and a thickened appendiceal wall, suggesting acute appendicitis.
(Enlarge Image)
Figure 4.
Contrast-enhanced computed tomographic scout view of the abdomen revealing the retrocecal region of the appendix with inflammation and mesenteric fat infiltration and a thickened appendiceal wall, suggesting acute appendicitis.
After consultation with the surgeons, the patient was emergently taken to the operating room. Exploratory laparotomy was performed. After opening the abdomen, 2000 ml of blood were removed immediately. Surgery showed splenic subcapsular rupture and intraperitoneal blood with an otherwise normal spleen. The appendix was also removed, showing an acutely inflamed and non-perforated appendix. The pathology report demonstrated the spleen to be mildly enlarged and the parenchyma to be normal. The rupture was found on the medial side, penetrating into the parenchyma of the spleen. Histopathological analysis of the appendectomy specimen revealed the presence of intense inflammatory infiltrate composed of neutrophils and leukocytes accompanied by abundant eosinophils, suggestive of Anisakis appendicitis (Figures 5 and 6). Upon interrogation approximately 3 weeks later, the patient reported intermittent crampy abdominal pain located in the right lower quadrant that radiated to the right flank and was associated with borborygmi and diarrhea. The diagnosis was confirmed later by the detection of Anisakis Deoxyribonucleic acid (DNA) in the resected appendix on the basis of nested polymerase chain reaction. Paired acute-phase and convalescent sera provided no evidence of acute viral infection, and cultures from blood, sputum, stool and urine were negative. Screening for autoantibodies was negative. The patient's hospital course was uneventful, and she was discharged on postoperative day 5.
(Enlarge Image)
Figure 5.
Microscopic histopathological examination of the appendectomy specimen revealing the presence of intense inflammatory infiltrate composed of neutrophils and leukocytes accompanied by abundant eosinophils, suggestive of Anisakis appendicitis.
(Enlarge Image)
Figure 6.
Microscopic histopathological examination of the appendectomy specimen revealing the presence of intense inflammatory infiltrate composed of neutrophils and leukocytes accompanied by abundant eosinophils, suggestive of Anisakis appendicitis.
The results of serologic testing during the patient's hospital course and after discharge were negative throughout, including tests for antibodies to varicella zoster virus IgG. The results of all the following tests were negative: syphilis; antibodies to Epstein-Barr virus IgG and IgM, cryptococcus, rickettsia and human immunodeficiency virus (HIV); antigens of cytomegalovirus (CMV); and nucleic acids of CMV and HIV. The following test results were normal: direct Coombs antibody test; cold agglutinin screening and testing for lupus anticoagulant; hemoglobin electrophoresis; and levels of fibrinogen, homocysteine, lipoprotein (a), β2-glycoprotein I, anti-thrombin III and protein C (functional). At the time of her current admission her total IgE level was 760 kU/l and her specific IgE against Anisakis simplex was > 100 kU/l. Two months later her IgE level was 221 kU/l, and her specific IgE against Anisakis simplex was 34 kU/l. An upper endoscopy examination was later performed. Macroscopic examination revealed signs of moderate inflammation of the gastric mucosa, and a gastric biopsy revealed small areas of granulation tissue that had evidence of eosinophilic leukocyte infiltration within the gastric muscularis layer. The patient currently remains on active duty at work, and at her 18-month follow-up she reported doing well since being discharged, with no known sequelae.
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