The Experts below are selected from a list of 606 Experts worldwide ranked by ideXlab platform
James M. Mckee - One of the best experts on this subject based on the ideXlab platform.
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Images in Emergency Medicine: Splenic Infarction Due to Sickle Cell Trait after Climbing Mt. Fuji
The western journal of emergency medicine, 2008Co-Authors: Aki Morishima, Joel M. Schofer, Pierre Pelletier, James M. MckeeAbstract:A 41-year-old African American female with a history of alcoholism in remission developed acute vomiting, chills, and severe left upper quadrant abdominal pain while climbing Mt. Fuji (Shizuoka Prefecture, Japan). She presented to a Japanese hospital and was diagnosed with cholelithiasis. The studies obtained are unknown and were unavailable. She presented two days later to a military emergency department in Okinawa, Japan (a two hour flight from Mt. Fuji) with continued severe left upper quadrant pain, increased with inspiration. Her only medication was disulfiram. The remainder of her history was unremarkable. Her vitals signs were normal, except for a blood pressure of 158/93 mm Hg. She appeared to be in moderate distress. Her physical examination was significant for Tenderness in the left upper quadrant with guarding but no rebound. She had left Costovertebral Angle Tenderness. Her urinalysis showed small blood on the urine dipstick with negative microscopy. A non-contrast CT scan of the abdomen and pelvis, obtained to look for urolithiasis, showed cholelithiasis. A contrast enhanced CT of the abdomen and pelvis was consistent with splenic infarction (Figure 1). Hemoglobin electrophoresis obtained upon admission was consistent with sickle cell trait. Splenic infarction in patients with sickle cell trait was first reported during the Korean War in African American pilots flying in unpressurizedaircraft.1 Figure 1 Contrast abdominal CT at the level of the splenic hilum shows lack of contrast enhancement in a large area of the anterior spleen. Patients with sickle cell trait inherit a normal hemoglobin A gene from one parent and an abnormal hemoglobin S gene from the other parent. In the United States, it occurs in 7–10% of African Americans and is rare in people of other ethnicities.2 Although patients with sickle cell trait are usually asymptomatic, they can develop splenic infarctions in hypoxic environments.3 Signs and symptoms typically include epigastric and left upper quadrant pain developing over 48 hours and may include guarding, rebound, splenomegaly, fever, anorexia, and vomiting. Laboratory data often show increases in lactate dehydrogenase, leukocystosis, thrombocytopenia, and anemia.1,2,3, A CT scan with intravenous contrast will demonstrate areas of multifocal splenic infarcts. Splenic rupture is a rare complication. Treatment with supportive care including oxygen, analgesia, and hydration is usually adequate. Patients who are unstable may require splenectomy.2 In this case, supportive care was provided and the patient recovered without sequelae. Physicians should consider splenic infarction in patients who develop suspicious symptoms after exposure to a high altitude environment.3
Aki Morishima - One of the best experts on this subject based on the ideXlab platform.
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Images in Emergency Medicine: Splenic Infarction Due to Sickle Cell Trait after Climbing Mt. Fuji
The western journal of emergency medicine, 2008Co-Authors: Aki Morishima, Joel M. Schofer, Pierre Pelletier, James M. MckeeAbstract:A 41-year-old African American female with a history of alcoholism in remission developed acute vomiting, chills, and severe left upper quadrant abdominal pain while climbing Mt. Fuji (Shizuoka Prefecture, Japan). She presented to a Japanese hospital and was diagnosed with cholelithiasis. The studies obtained are unknown and were unavailable. She presented two days later to a military emergency department in Okinawa, Japan (a two hour flight from Mt. Fuji) with continued severe left upper quadrant pain, increased with inspiration. Her only medication was disulfiram. The remainder of her history was unremarkable. Her vitals signs were normal, except for a blood pressure of 158/93 mm Hg. She appeared to be in moderate distress. Her physical examination was significant for Tenderness in the left upper quadrant with guarding but no rebound. She had left Costovertebral Angle Tenderness. Her urinalysis showed small blood on the urine dipstick with negative microscopy. A non-contrast CT scan of the abdomen and pelvis, obtained to look for urolithiasis, showed cholelithiasis. A contrast enhanced CT of the abdomen and pelvis was consistent with splenic infarction (Figure 1). Hemoglobin electrophoresis obtained upon admission was consistent with sickle cell trait. Splenic infarction in patients with sickle cell trait was first reported during the Korean War in African American pilots flying in unpressurizedaircraft.1 Figure 1 Contrast abdominal CT at the level of the splenic hilum shows lack of contrast enhancement in a large area of the anterior spleen. Patients with sickle cell trait inherit a normal hemoglobin A gene from one parent and an abnormal hemoglobin S gene from the other parent. In the United States, it occurs in 7–10% of African Americans and is rare in people of other ethnicities.2 Although patients with sickle cell trait are usually asymptomatic, they can develop splenic infarctions in hypoxic environments.3 Signs and symptoms typically include epigastric and left upper quadrant pain developing over 48 hours and may include guarding, rebound, splenomegaly, fever, anorexia, and vomiting. Laboratory data often show increases in lactate dehydrogenase, leukocystosis, thrombocytopenia, and anemia.1,2,3, A CT scan with intravenous contrast will demonstrate areas of multifocal splenic infarcts. Splenic rupture is a rare complication. Treatment with supportive care including oxygen, analgesia, and hydration is usually adequate. Patients who are unstable may require splenectomy.2 In this case, supportive care was provided and the patient recovered without sequelae. Physicians should consider splenic infarction in patients who develop suspicious symptoms after exposure to a high altitude environment.3
Pierre Pelletier - One of the best experts on this subject based on the ideXlab platform.
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Images in Emergency Medicine: Splenic Infarction Due to Sickle Cell Trait after Climbing Mt. Fuji
The western journal of emergency medicine, 2008Co-Authors: Aki Morishima, Joel M. Schofer, Pierre Pelletier, James M. MckeeAbstract:A 41-year-old African American female with a history of alcoholism in remission developed acute vomiting, chills, and severe left upper quadrant abdominal pain while climbing Mt. Fuji (Shizuoka Prefecture, Japan). She presented to a Japanese hospital and was diagnosed with cholelithiasis. The studies obtained are unknown and were unavailable. She presented two days later to a military emergency department in Okinawa, Japan (a two hour flight from Mt. Fuji) with continued severe left upper quadrant pain, increased with inspiration. Her only medication was disulfiram. The remainder of her history was unremarkable. Her vitals signs were normal, except for a blood pressure of 158/93 mm Hg. She appeared to be in moderate distress. Her physical examination was significant for Tenderness in the left upper quadrant with guarding but no rebound. She had left Costovertebral Angle Tenderness. Her urinalysis showed small blood on the urine dipstick with negative microscopy. A non-contrast CT scan of the abdomen and pelvis, obtained to look for urolithiasis, showed cholelithiasis. A contrast enhanced CT of the abdomen and pelvis was consistent with splenic infarction (Figure 1). Hemoglobin electrophoresis obtained upon admission was consistent with sickle cell trait. Splenic infarction in patients with sickle cell trait was first reported during the Korean War in African American pilots flying in unpressurizedaircraft.1 Figure 1 Contrast abdominal CT at the level of the splenic hilum shows lack of contrast enhancement in a large area of the anterior spleen. Patients with sickle cell trait inherit a normal hemoglobin A gene from one parent and an abnormal hemoglobin S gene from the other parent. In the United States, it occurs in 7–10% of African Americans and is rare in people of other ethnicities.2 Although patients with sickle cell trait are usually asymptomatic, they can develop splenic infarctions in hypoxic environments.3 Signs and symptoms typically include epigastric and left upper quadrant pain developing over 48 hours and may include guarding, rebound, splenomegaly, fever, anorexia, and vomiting. Laboratory data often show increases in lactate dehydrogenase, leukocystosis, thrombocytopenia, and anemia.1,2,3, A CT scan with intravenous contrast will demonstrate areas of multifocal splenic infarcts. Splenic rupture is a rare complication. Treatment with supportive care including oxygen, analgesia, and hydration is usually adequate. Patients who are unstable may require splenectomy.2 In this case, supportive care was provided and the patient recovered without sequelae. Physicians should consider splenic infarction in patients who develop suspicious symptoms after exposure to a high altitude environment.3
Joel M. Schofer - One of the best experts on this subject based on the ideXlab platform.
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Images in Emergency Medicine: Splenic Infarction Due to Sickle Cell Trait after Climbing Mt. Fuji
The western journal of emergency medicine, 2008Co-Authors: Aki Morishima, Joel M. Schofer, Pierre Pelletier, James M. MckeeAbstract:A 41-year-old African American female with a history of alcoholism in remission developed acute vomiting, chills, and severe left upper quadrant abdominal pain while climbing Mt. Fuji (Shizuoka Prefecture, Japan). She presented to a Japanese hospital and was diagnosed with cholelithiasis. The studies obtained are unknown and were unavailable. She presented two days later to a military emergency department in Okinawa, Japan (a two hour flight from Mt. Fuji) with continued severe left upper quadrant pain, increased with inspiration. Her only medication was disulfiram. The remainder of her history was unremarkable. Her vitals signs were normal, except for a blood pressure of 158/93 mm Hg. She appeared to be in moderate distress. Her physical examination was significant for Tenderness in the left upper quadrant with guarding but no rebound. She had left Costovertebral Angle Tenderness. Her urinalysis showed small blood on the urine dipstick with negative microscopy. A non-contrast CT scan of the abdomen and pelvis, obtained to look for urolithiasis, showed cholelithiasis. A contrast enhanced CT of the abdomen and pelvis was consistent with splenic infarction (Figure 1). Hemoglobin electrophoresis obtained upon admission was consistent with sickle cell trait. Splenic infarction in patients with sickle cell trait was first reported during the Korean War in African American pilots flying in unpressurizedaircraft.1 Figure 1 Contrast abdominal CT at the level of the splenic hilum shows lack of contrast enhancement in a large area of the anterior spleen. Patients with sickle cell trait inherit a normal hemoglobin A gene from one parent and an abnormal hemoglobin S gene from the other parent. In the United States, it occurs in 7–10% of African Americans and is rare in people of other ethnicities.2 Although patients with sickle cell trait are usually asymptomatic, they can develop splenic infarctions in hypoxic environments.3 Signs and symptoms typically include epigastric and left upper quadrant pain developing over 48 hours and may include guarding, rebound, splenomegaly, fever, anorexia, and vomiting. Laboratory data often show increases in lactate dehydrogenase, leukocystosis, thrombocytopenia, and anemia.1,2,3, A CT scan with intravenous contrast will demonstrate areas of multifocal splenic infarcts. Splenic rupture is a rare complication. Treatment with supportive care including oxygen, analgesia, and hydration is usually adequate. Patients who are unstable may require splenectomy.2 In this case, supportive care was provided and the patient recovered without sequelae. Physicians should consider splenic infarction in patients who develop suspicious symptoms after exposure to a high altitude environment.3
Marshall L. Stoller - One of the best experts on this subject based on the ideXlab platform.
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Randall plaque versus renal stone
Translational andrology and urology, 2012Co-Authors: Thomas Chi, Joe Miller, Marshall L. StollerAbstract:A 43-year-old patient has just left the office. Her primary care physician had dutifully evaluated her recent complaint of vague abdominal pain with an abdominal ultrasound. The multiple, small, punctate hyperechoic lesions in the kidney were deemed concerning for renal calculi and an abdominal computed tomography (CT) scan was ordered to better delineate these "renal stones". The CT report revealed " multiple bilateral punctate calcifications consistent with possible nephrolithiasis versus nephrocalcinosis ," and the patient was referred to urology clinic for further evaluation. In our clinic the patient was interviewed and examined and the scan was carefully reviewed. The patient denied symptoms of renal colic and physical examination demonstrated no Costovertebral Angle Tenderness. No hydronephrosis or evidence of urinary obstruction could be seen on the scan, and we provided a diagnosis of Randall plaques and nephrocalcinosis. The patient was reassured that there were no stones to treat and there was no need for surgery. General lifestyle and dietary modification counseling for stone prevention were provided, and the patient was discharged from our clinic, happy with her benign diagnosis.
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Bilateral Renal-Vein Thrombosis Associated with the Nephrotic Syndrome
The New England journal of medicine, 2006Co-Authors: Surat Phonsombat, Marshall L. StollerAbstract:A 61-year-old woman whose medical history was notable for hypertension and type 2 diabetes reported a two-day history of increasing dull pain in the right flank and nonbloody, bilious vomiting. Physical examination revealed no abdominal masses, Costovertebral-Angle Tenderness, or peripheral edema. Laboratory evaluation revealed normal serum creatinine levels (1.0 mg per deciliter [88.4 μmol per liter]); the presence of hyperlipidemia (total cholesterol level, 938 mg per deciliter [24.3 mmol per liter]; triglyceride level, 811 mg per deciliter [9.2 mmol per liter]; and high-density lipoprotein cholesterol level, 44 mg per deciliter [1.1 mmol per liter]); low total-protein and albumin levels (3.9 . . .
