Post-transfusion purpura (PTP) is a rare disease characterized by life-threatening thrombocytopenia after transfusion of any platelet-containing blood products, such as platelets(PLT) or packed red blood cells (PRBCs). We report an interesting case of PTP in a young lady after receiving multiple blood products. CASE PRESENTATION:A 36-year-old female with a past medical history of diabetes mellitus and left-sided below-knee amputation (BKA) was admitted to the Intensive Care Unit (ICU) for emphysematous osteomyelitis with intraosseous gas in the calcaneus, cuboid, and fifth metatarsal base of the right lower extremity. She underwent right-sided BKA, requiring multiple PRBC transfusions due to a combination of blood loss during surgery and chronic anemia. The initial platelet count was normal at 329,000/uL. Five days after the PRBC transfusion, it trended down to 17,000/uL and there was concurrent development of a purpuric rash over both arms. Bloodwork was notable for elevated prothrombin time and activated partial thromboplastin time. Hemolysis workup and Coombs test were negative. Fibrinogen was elevated, ruling out disseminated intravascular coagulation. PTP was suspected based on the clinical presentation and exclusion of other etiologies. Anti-human platelet antigen-1a (HPA-1a) antibodies were obtained. Empiric treatment with intravenous immunoglobulin (IVIG) and steroids was promptly initiated. Platelet count improved to 157,000/uL after four doses of IVIG. The patient tested positive for HPA-1a. However, due to the urgent need for treatment, the test sample for the anti-platelet antibodies was drawn after the initiation of IVIG. The development of thrombocytopenia in the classic time frame with the characteristic rash and improvement after receiving IVIG make PTP the most likely diagnosis. She was recommended to receive only washed PRBCs in the future to prevent a recurrence. DISCUSSION: PTP is a rare, underdiagnosed, and potentially fatal reaction, with the development of severe thrombocytopenia 2-14 days after transfusion of platelet-containing blood products. It is considered to be caused by alloimmunization against platelet antigens, with HPA-1a being the most common antibody1. Some cases of HPA-1b mediated PTP have been reported as well2. Diagnosis is often subtle and challenging, therefore a strong clinical suspicion is needed. A history of blood product transfusion a few days before the development of thrombocytopenia should make the physician think about the possibility of PTP. Treatment includes IVIG, steroids, or plasmapheresis3, and initiation of treatment should not wait for diagnostic confirmation.CONCLUSIONS: Clinicians should have high clinical suspicion for PTP in patients with acute, severe thrombocytopenia which develops after blood transfusions, and treatment should be initiated early to favorably alter the course of the disease.
INTRODUCTION: Lady Windermere syndrome(LWS) was described first in 1989 when a series of patients with M.Avium complex(MAC) disease without predisposing factors were reported1. The disease commonly occurs in immunocompetent elderly women with no prior lung disease and involves the right middle lobe(RML) and lingula. It is related to a habit of voluntary cough suppression2 and was named based on Oscar Wilde's character in "Lady Windermere's fan."I describe here the case of three sisters with no past medical history who were diagnosed as having LWS. There have been no case reports of this syndrome affecting members of the same family.CASE PRESENTATION: Patient 1:A 43-year-old female presented with a history of productive cough for 20 years. She also complained of fever, night sweats, decreased appetite, and marked weight loss over two years. There was no history of hemoptysis. The blood count showed mild leukocytosis with prominent neutrophilia. Sputum for acid-fast bacilli(AFB) was negative. Chest xray(CXR) showed nonspecific changes in the left apex and both lower zones. CT scan of the chest showed marked bronchiectasis of the RML and mild lingular changes.Patient 2:A 47-year-old female presented with a history of productive cough for 15 years with off and on hemoptysis and marked weight loss. CXR showed infiltrates in RML and opacity in the left paracardiac region. CT scan of the chest showed early bronchiectatic changes in the RML and lingula. Segmental and subsegmental bronchi were dilated. Bronchial washing cultures were negative for AFB and fungus.Patient 3:A 55-year-old female presented with a history of productive cough for 25 years with off and on hemoptysis and marked weight loss. Sputum for AFB was negative. CT scan of the chest showed dense patchy, nodular, and fibrocystic opacities along with bronchiectatic changes in the RML and lingula. Bronchial washing cultures for AFB and fungus were negative.DISCUSSION: Habitual cough suppression leads to retained secretions in the long, narrow bronchi subserving RML and lingula. Consequent chronic low-grade inflammation upon which MAC may engraft results in regional bronchiectasis. In our cases, the diagnosis of LWS was based on the characteristic radiographic findings and the fact that there was symptomatic improvement when all three were treated with anti-tuberculous therapy. CONCLUSIONS:Although conventionally, LWS is not considered to spread person to person3, these cases might make one wonder if there are exceptions under certain environmental and genetic conditions.
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INTRODUCTION: Burkitt lymphoma (BL) is a highly aggressive non-Hodgkin B-cell lymphoma that typically presents with multiple metabolic derangements, kidney failure, involvement of the jaw or other facial bones, and enlarged lymph nodes. Our case report describes an initial presentation of (BL) with septic shock.CASE PRESENTATION: 25-year-old Caucasian female presented with a 4-day history of sharp non-radiating right upper quadrant abdominal pain, poor appetite, nausea, multiple episodes of loose watery stools, and polydipsia. Exam was notable for 2/ 4 SIRS criteria, with heart rate 134 and respiratory rate 29, and right upper quadrant was tender to palpation. Workup revealed white blood cell count 10.3 thou/uL, lactate 4.
Pyogenic liver abscess (PLA) is a rare complication of diabetes, associated with poor glycemic control, and can potentially be life-threatening. We present a case of resistant diabetic ketoacidosis found to have underlying PLA.CASE PRESENTATION: 49-year-old male with past medical history of insulin-dependent diabetes mellitus presented with several days of malaise, nausea, and vomiting. Vital signs were notable for tachycardia and tachypnea, with physical exam notable for mild epigastric tenderness. Labwork was notable for white blood cell count 24.7 thou/uL with neutrophilic predominance, blood glucose of 496 with increased anion gap (30) metabolic acidosis (pH 7.17), beta-hydroxybutyric acid 11.10 mmol/L, lactic acid 4.9 mmol/L, and ketonuria. Transaminitis was also noted: aspartate aminotransferase (AST) 81 U/L, alanine aminotransferase (ALT) 74 U/L, and alkaline phosphatase 147 U/L. He was admitted for management of diabetic ketoacidosis requiring frequent accu-checks and an insulin drip. His blood sugars were hard to control and given persistent leukocytosis, imaging was obtained, with computed tomography (CT) of chest/abdomen/pelvis showed confluent liver masses, most compatible with liver abscesses. Liver ultrasound confirmed the diagnosis of multiple liver abscesses, therefore the patient was placed on broad-spectrum antibiotics. A thorough workup was done to determine the etiology of the abscesses, however, it was unremarkable; therefore, the etiology was thought to most likely be suppressed immunity secondary to poor diabetic control, with hemoglobin A1C of 14%, in addition to elevated blood sugars for a prolonged period leading to abscess formation. Subsequently, 4/4 blood cultures were consistent with Escherichia coli (E. coli) bacteremia. He underwent drainage of the abscesses with placement of 2 pigtail drainage catheters; culture of the fluid was also positive for E. coli infection. With control of the infection, blood sugar control was also achieved, and the patient was transitioned to an insulin regimen prior to discharge with oral antibiotics and extensive diabetic education.DISCUSSION: PLA is a supportive infection involving the hepatic parenchyma, mostly seen in Asian countries, with its incidence in the USA very rare, seen in about 3.59 per 100,000 cases [1]. Risk factors include autoimmune disease, cholangitis, malignancy, and diabetes mellitus among others, with recent studies showing increased morbidity in patients with PLA secondary to diabetes. Klebsiella pneumonia is the organism most commonly found to be the culprit, followed by E. coli [2]. While the bacteria usually remains confined to the liver, the risk for bacteremia is increased in patients with uncontrolled diabetes [1].CONCLUSIONS: Clinicians should maintain a high clinical suspicion for PLA, especially in those presenting with DKA and concurrent transaminitis as early treatment can improve outcomes.
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