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Spontaneous Splenic Infarction as an Uncommon Cause of Fever in a Cirrhotic Patient
International Journal of Gerontology 11 (2017) 121e124
Contents lists available at ScienceDirect
International Journal of Gerontology journal homepage: www.ijge-online.com
Case Report
Spontaneous Splenic Infarction as an Uncommon Cause of Fever in a Cirrhotic Patient Chun-Han Cheng a, Ming-Jong Bair a, b, c * a Division of Gastroenterology, Department of Internal Medicine, Taitung Mackay Memorial Hospital, Taiwan, Taiwan, c Department of Nursing, Meiho University, Taitung, Taiwan
b
Mackay Medical College, New Taipei,
a r t i c l e i n f o
s u m m a r y
Article history: Received 25 May 2016 Received in revised form 3 August 2016 Accepted 30 September 2016 Available online 23 May 2017
Spontaneous splenic infarction is a relative rare disease and usually happens in patients with some disorders that have potential of thromboembolism formation. The symptoms are often subclinical and non-specific so physicians easily forget this diagnosis. However, splenic infarction could cause destructive consequences such as hemorrhagic shock, especially in old or weak patients. In this article, we present one case with fever and unexplained abdominal pain; the patient was ultimately diagnosed spontaneous splenic infarction. Although early suspicion or diagnosis may be challenged, physicians should remember this disease and arrange associated investigation to make correct management. Copyright © 2017, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Keywords: splenic infarction, cirrhosis
1. Introduction Spontaneous splenic infarction refers to a condition that oxygen supply of the spleen is interrupted due to occlusion of the splenic vascular or its branches, leading to parenchymal ischemia. The clinical spectrum ranges from asymptomatic disease, splenic abscess, to hemorrhagic shock. It frequently occurs in patients with specific underlying disease (myeloproliferative disorders, malignancy, atrial fibrillation…etc).1 We presented one old-aged cirrhotic patient who diagnosed splenic infarction without common etiologies.
2. Case report A 72-year-old female was previously diagnosed with cirrhosis and splenomegaly. She was admitted for fever and chills for 5 days. The patient's temperature was measured up to 39.1 C. There were no obvious gastrointestinal complaints such as abdominal pain, vomiting, anorexia, dysphagia, constipation, diarrhea, and tarry stool. Physical examination demonstrated mild left abdominal tenderness without muscle guarding or rebounding tenderness. The white cell counts were 10900/mL (normal range: 4000e10000/
mL) and the neutrophils account for 91.0%. The C-reactive protein was 6.578 mg/dL (normal range: 0.000e0.748 mg/dL). Initial fever work up including chest radiography and urinalysis were unremarkable. The abdominal echogram showed wedge-shape heterogenous hypoechoic lesions in spleen (Fig. 1). The abdominal computed tomography (CT) revealed one well-demarcated lowdensity area in spleen, favoring splenic infarction (Fig. 2). We suspected the diagnosis of secondary splenic abscess formation according to the clinical manifestation and heterogenous characteristics in echogram image. The patient didn't have evidence of hematological malignancy. The results of blood protein C, protein S, anti-nuclear antibody were normal. The electrocardiogram displayed normal sinus rhythm without atrial fibrillation and echocardiography didn't demonstrate vegetation. We prescribed intravenous antibiotics piperacillin/tazobactam, fluid supply and acetaminophen for fever control. We didn't insert the drainage tube and just closely followed abdominal echogram. After supportive care and medical treatment, the size of lesion decreased and the patient was discharged smoothly. The total duration of hospitalization was 17 days. After discharged, we followed abdominal echogram and CT, which demonstrated regression of the lesion size (Fig. 3). 3. Discussions
* Correspondence to: Ming-Jong Bair, Division of Gastroenterology, Department of Internal Medicine, Taitung Mackay Memorial Hospital, Taiwan. E-mail address: [email protected] (M.-J. Bair).
Splenic infarction is a relative uncommon disease. The arterial supply of the spleen consists of the splenic artery and short gastric
http://dx.doi.org/10.1016/j.ijge.2016.09.005 1873-9598/Copyright © 2017, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
122
C.-H. Cheng, M.-J. Bair
Fig. 1. The abdominal echogram showed heterogenous hypoechoic lesions in the spleen.
arteries. The splenic artery divided into 4e5 branches before entering the spleen; each branch supplies a functionally separate segment.2 Therefore, segmental infarction would happen if one or more branches of splenic artery were occlusion by any cause.3 There are numerous etiologies of splenic infarction. The most common are hematological disorders leading to hypercoagulable states, such as myeloproliferative disorders, leukemia, sickle cell disease, protein C or protein S deficiency, lupus anticoagulant, etc.4,5 Other malignancy and splenic infection (infectious mononucleosis, cytomegalovirus infection) may increase the tendency for clot formation.6 Some embolic disorders (endocarditis, atrial fibrillation) could form blood clots in systemic circulation and cause splenic infarction.7 Trauma to the spleen, which compromises its vascularity, may also contribute to disruption of splenic blood
supply. In our article, the patient didn't have any evidences of above problems. However, liver cirrhosis with portal hypertension is known one of the common causes of hypercoagulable status and may leading higher tendency of thrombus formation. Sometimes, the diagnosis of splenic infarction was the clue that the patient may have other serious underlying diseases such as hypercoagulable state, atrial fibrillation…etc.1 The clinical manifestation of splenic infarction ranges from asymptomatic disease, splenic abscess, to hemorrhagic shock.8 Abdominal pain, especially at left upper quadrant area was the most common symptoms of splenic infarction, followed by fever/ chills, nausea and vomiting. The most frequent signs are left upper quadrate tenderness, leukocytosis, and increased lactate dehydrogenase.1,3 Approximately 30% patients of splenic infarction are
Splenic Infarction in a Cirrhotic Patient
123
Fig. 3. The followed abdominal CT revealed that the lesion size decreased (arrow).
Fig. 2. The transverse (upper) and coronal view (lower) of abdominal CT demonstrated a well-demarcated low-density area in spleen (arrow), favoring massive splenic infarction.
clinically occult. Due to non-specific symptoms and signs, the clinical presentation of splenic infarction may mimic other diseases causing abdominal pain and fever. In present article, the patient only complained fever and chills without other common symptoms. Early diagnosis of splenic infarction may be difficult in these patients. The diagnosis is based on clinical characteristics and splenic image. The laboratory studies for splenic infarction are nonspecific. The image on abdominal sonography frequently appears as a focal wedge-shape, hypoechoic, well-demarcated lesions. Abdominal computed tomography with intravenous contrast is frequently used to diagnose splenic infarction. The typical features are clearly, segmental, wedge-shape, low-density defects in the spleen. Contrast-enhancing imaging studies should be considered in patients with unexplained abdominal pain, even without obvious risk factors of splenic infarction. The treatment is mostly conservative. The mainstay of nonoperative therapy is analgesia and close follow-up. It is important to trace underlying diseases and to apply further management.
Surgery is indicated only in the presence of complications, such as bleeding, pseudocyst formation, and massive abscess. Smaller pseudocysts usually regress spontaneously but larger cysts often require intervention.9 Small splenic abscess can be treated with antibiotics alone or simultaneous percutaneous drainage. In patients with larger, multiple splenic abscess, surgery are usually necessary. In conclusion, we should keep in mind that splenic infarction is a relative rare disease but could happen in cirrhotic patients. Further imaging study in patients with unexplained abdominal pain is important to avoid potentially fatal diseases. In patients who diagnosed splenic infarction, investigation of uncovered underlying diagnosis is necessary. Statement The content of the manuscript is original and it has not been published or accepted for publication, either in whole or in part, in any form. No part of the manuscript is currently under consideration for publication elsewhere. References 1. Antopolsky M, Hiller N, Salameh S, et al. Splenic infarction: 10 years of experience. Am J Emerg Med. 2009 Mar;27(3):262e265. 2. Sadler TW. Chapter 14: Digestive System. Langman's Medical Embryology. 11th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2009:215e216. 3. Lawrence YR, Pokroy R, Berlowitz D, et al. Splenic infarction: an update on William Osler's observations. Isr Med Assoc J. 2010 Jun;12(6):362e365.
124 4. Olson JF, Steuber CP, Hawkins E, et al. Functional deficiency of protein C associated with mesenteric venous thrombosis and splenic infarction. Am J Pediatr Hematol Oncol. 1991 Summer;13(2):168e171. 5. Ebert EC, Nagar M, Hagspiel KD. Gastrointestinal and hepatic complications of sickle cell disease. Clin Gastroenterol Hepatol. 2010 Jun;8(6):483e489. 6. van Hal S, Senanayake S, Hardiman R. Splenic infarction due to transient antiphospholipid antibodies induced by acute Epstein-Barr virus infection. J Clin Virol. 2005 Mar;32(3):245e247.
C.-H. Cheng, M.-J. Bair 7. Ting W, Silverman NA, Arzouman DA, et al. Splenic septic emboli in endocarditis. Circulation. 1990 Nov;82(5 Suppl). IV105e9. 8. Nores M, Phillips EH, Morgenstern L, et al. The clinical spectrum of splenic infarction. Am Surg. 1998 Feb;64(2):182e188. 9. Pachter HL, Hofstetter SR, Elkowitz A. Traumatic cysts of the spleenethe role of cystectomy and splenic preservation: experience with seven consecutive patients. J Trauma. 1993 Sep;35(3):430e436.
Contents lists available at ScienceDirect
International Journal of Gerontology journal homepage: www.ijge-online.com
Case Report
Spontaneous Splenic Infarction as an Uncommon Cause of Fever in a Cirrhotic Patient Chun-Han Cheng a, Ming-Jong Bair a, b, c * a Division of Gastroenterology, Department of Internal Medicine, Taitung Mackay Memorial Hospital, Taiwan, Taiwan, c Department of Nursing, Meiho University, Taitung, Taiwan
b
Mackay Medical College, New Taipei,
a r t i c l e i n f o
s u m m a r y
Article history: Received 25 May 2016 Received in revised form 3 August 2016 Accepted 30 September 2016 Available online 23 May 2017
Spontaneous splenic infarction is a relative rare disease and usually happens in patients with some disorders that have potential of thromboembolism formation. The symptoms are often subclinical and non-specific so physicians easily forget this diagnosis. However, splenic infarction could cause destructive consequences such as hemorrhagic shock, especially in old or weak patients. In this article, we present one case with fever and unexplained abdominal pain; the patient was ultimately diagnosed spontaneous splenic infarction. Although early suspicion or diagnosis may be challenged, physicians should remember this disease and arrange associated investigation to make correct management. Copyright © 2017, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Keywords: splenic infarction, cirrhosis
1. Introduction Spontaneous splenic infarction refers to a condition that oxygen supply of the spleen is interrupted due to occlusion of the splenic vascular or its branches, leading to parenchymal ischemia. The clinical spectrum ranges from asymptomatic disease, splenic abscess, to hemorrhagic shock. It frequently occurs in patients with specific underlying disease (myeloproliferative disorders, malignancy, atrial fibrillation…etc).1 We presented one old-aged cirrhotic patient who diagnosed splenic infarction without common etiologies.
2. Case report A 72-year-old female was previously diagnosed with cirrhosis and splenomegaly. She was admitted for fever and chills for 5 days. The patient's temperature was measured up to 39.1 C. There were no obvious gastrointestinal complaints such as abdominal pain, vomiting, anorexia, dysphagia, constipation, diarrhea, and tarry stool. Physical examination demonstrated mild left abdominal tenderness without muscle guarding or rebounding tenderness. The white cell counts were 10900/mL (normal range: 4000e10000/
mL) and the neutrophils account for 91.0%. The C-reactive protein was 6.578 mg/dL (normal range: 0.000e0.748 mg/dL). Initial fever work up including chest radiography and urinalysis were unremarkable. The abdominal echogram showed wedge-shape heterogenous hypoechoic lesions in spleen (Fig. 1). The abdominal computed tomography (CT) revealed one well-demarcated lowdensity area in spleen, favoring splenic infarction (Fig. 2). We suspected the diagnosis of secondary splenic abscess formation according to the clinical manifestation and heterogenous characteristics in echogram image. The patient didn't have evidence of hematological malignancy. The results of blood protein C, protein S, anti-nuclear antibody were normal. The electrocardiogram displayed normal sinus rhythm without atrial fibrillation and echocardiography didn't demonstrate vegetation. We prescribed intravenous antibiotics piperacillin/tazobactam, fluid supply and acetaminophen for fever control. We didn't insert the drainage tube and just closely followed abdominal echogram. After supportive care and medical treatment, the size of lesion decreased and the patient was discharged smoothly. The total duration of hospitalization was 17 days. After discharged, we followed abdominal echogram and CT, which demonstrated regression of the lesion size (Fig. 3). 3. Discussions
* Correspondence to: Ming-Jong Bair, Division of Gastroenterology, Department of Internal Medicine, Taitung Mackay Memorial Hospital, Taiwan. E-mail address: [email protected] (M.-J. Bair).
Splenic infarction is a relative uncommon disease. The arterial supply of the spleen consists of the splenic artery and short gastric
http://dx.doi.org/10.1016/j.ijge.2016.09.005 1873-9598/Copyright © 2017, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
122
C.-H. Cheng, M.-J. Bair
Fig. 1. The abdominal echogram showed heterogenous hypoechoic lesions in the spleen.
arteries. The splenic artery divided into 4e5 branches before entering the spleen; each branch supplies a functionally separate segment.2 Therefore, segmental infarction would happen if one or more branches of splenic artery were occlusion by any cause.3 There are numerous etiologies of splenic infarction. The most common are hematological disorders leading to hypercoagulable states, such as myeloproliferative disorders, leukemia, sickle cell disease, protein C or protein S deficiency, lupus anticoagulant, etc.4,5 Other malignancy and splenic infection (infectious mononucleosis, cytomegalovirus infection) may increase the tendency for clot formation.6 Some embolic disorders (endocarditis, atrial fibrillation) could form blood clots in systemic circulation and cause splenic infarction.7 Trauma to the spleen, which compromises its vascularity, may also contribute to disruption of splenic blood
supply. In our article, the patient didn't have any evidences of above problems. However, liver cirrhosis with portal hypertension is known one of the common causes of hypercoagulable status and may leading higher tendency of thrombus formation. Sometimes, the diagnosis of splenic infarction was the clue that the patient may have other serious underlying diseases such as hypercoagulable state, atrial fibrillation…etc.1 The clinical manifestation of splenic infarction ranges from asymptomatic disease, splenic abscess, to hemorrhagic shock.8 Abdominal pain, especially at left upper quadrant area was the most common symptoms of splenic infarction, followed by fever/ chills, nausea and vomiting. The most frequent signs are left upper quadrate tenderness, leukocytosis, and increased lactate dehydrogenase.1,3 Approximately 30% patients of splenic infarction are
Splenic Infarction in a Cirrhotic Patient
123
Fig. 3. The followed abdominal CT revealed that the lesion size decreased (arrow).
Fig. 2. The transverse (upper) and coronal view (lower) of abdominal CT demonstrated a well-demarcated low-density area in spleen (arrow), favoring massive splenic infarction.
clinically occult. Due to non-specific symptoms and signs, the clinical presentation of splenic infarction may mimic other diseases causing abdominal pain and fever. In present article, the patient only complained fever and chills without other common symptoms. Early diagnosis of splenic infarction may be difficult in these patients. The diagnosis is based on clinical characteristics and splenic image. The laboratory studies for splenic infarction are nonspecific. The image on abdominal sonography frequently appears as a focal wedge-shape, hypoechoic, well-demarcated lesions. Abdominal computed tomography with intravenous contrast is frequently used to diagnose splenic infarction. The typical features are clearly, segmental, wedge-shape, low-density defects in the spleen. Contrast-enhancing imaging studies should be considered in patients with unexplained abdominal pain, even without obvious risk factors of splenic infarction. The treatment is mostly conservative. The mainstay of nonoperative therapy is analgesia and close follow-up. It is important to trace underlying diseases and to apply further management.
Surgery is indicated only in the presence of complications, such as bleeding, pseudocyst formation, and massive abscess. Smaller pseudocysts usually regress spontaneously but larger cysts often require intervention.9 Small splenic abscess can be treated with antibiotics alone or simultaneous percutaneous drainage. In patients with larger, multiple splenic abscess, surgery are usually necessary. In conclusion, we should keep in mind that splenic infarction is a relative rare disease but could happen in cirrhotic patients. Further imaging study in patients with unexplained abdominal pain is important to avoid potentially fatal diseases. In patients who diagnosed splenic infarction, investigation of uncovered underlying diagnosis is necessary. Statement The content of the manuscript is original and it has not been published or accepted for publication, either in whole or in part, in any form. No part of the manuscript is currently under consideration for publication elsewhere. References 1. Antopolsky M, Hiller N, Salameh S, et al. Splenic infarction: 10 years of experience. Am J Emerg Med. 2009 Mar;27(3):262e265. 2. Sadler TW. Chapter 14: Digestive System. Langman's Medical Embryology. 11th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2009:215e216. 3. Lawrence YR, Pokroy R, Berlowitz D, et al. Splenic infarction: an update on William Osler's observations. Isr Med Assoc J. 2010 Jun;12(6):362e365.
124 4. Olson JF, Steuber CP, Hawkins E, et al. Functional deficiency of protein C associated with mesenteric venous thrombosis and splenic infarction. Am J Pediatr Hematol Oncol. 1991 Summer;13(2):168e171. 5. Ebert EC, Nagar M, Hagspiel KD. Gastrointestinal and hepatic complications of sickle cell disease. Clin Gastroenterol Hepatol. 2010 Jun;8(6):483e489. 6. van Hal S, Senanayake S, Hardiman R. Splenic infarction due to transient antiphospholipid antibodies induced by acute Epstein-Barr virus infection. J Clin Virol. 2005 Mar;32(3):245e247.
C.-H. Cheng, M.-J. Bair 7. Ting W, Silverman NA, Arzouman DA, et al. Splenic septic emboli in endocarditis. Circulation. 1990 Nov;82(5 Suppl). IV105e9. 8. Nores M, Phillips EH, Morgenstern L, et al. The clinical spectrum of splenic infarction. Am Surg. 1998 Feb;64(2):182e188. 9. Pachter HL, Hofstetter SR, Elkowitz A. Traumatic cysts of the spleenethe role of cystectomy and splenic preservation: experience with seven consecutive patients. J Trauma. 1993 Sep;35(3):430e436.