Severe hypokalemia with cardiac arrest as an unusual manifestation of alcoholism

Introduction: Unhealthy use of alcohol can be associated with serious adverse events. Patients with alcoholism and malnutrition are at high risk for electrolyte disturbances, commonly hypokalemia. Here in we describe a case of alcohol use disorder presented with weakness and subsequently developed cardiac arrest secondary to severe hypokalemia. Case description: A 51-year-old lady presented to our emergency department because of generalized body ache and marked weakness in both lower extremities for two days duration. She had a long-term history of alcoholism, consuming two to three pints of vodka every day for about 20 years. Her last drink of alcohol was about 48 hours prior to presentation. Her examination revealed bilateral lower limb weakness of 4/5, with intact sensory system and reflexes. Biochemical analysis of the serum showed severe electrolytes disturbance, a potassium level of 2.3 mmol/L (reference 3.6−5.1 mmol/L). Electrocardiogram (ECG) showed no arrhythmias, but changes characteristic of hypokalemia with marked corrected QT segment prolongation (QTc 551ms). Aggressive supplementation of electrolytes was initiated, however, potassium level failed to increase and subsequently she had a sinus bradycardia followed by cardiac arrest. Cardiopulmonary resuscitation was initiated, return of spontaneous circulation was obtained. During the following days, potassium supplementation was continued to achieve normal plasma potassium level. She was then discharged from the hospital with recommendations for abstinence from alcohol. Conclusion: Patients with chronic alcohol-use can have serious electrolyte disturbances including hypokalemia which can have life-threatening consequences. Prolonged potassium supplementation over several days is required to achieve normal level of plasma potassium and replenish total-body potassium deficit

An unusual case of bilateral pulmonary embolism in a patient on dual venous thromboprophylaxis, secondary to heparin induced thrombocytopenia

Heparin Induced thrombocytopenia (HIT) is a rare, immune-mediated complication of heparin, associated with both thrombocytopenia and paradoxical thrombotic events. Initial diagnosis is made clinically when platelet count falls by 30% to  50% decrease from baseline count in association with heparin therapy. Thromboembolic complications are seen in 50% of the cases. We present a case of acute pulmonary embolism (aPE) in a 65 year old male secondary to HIT while on unfractionated heparin for venous thromboprophylaxis. He was admitted to the hospital for severe acute exacerbation of asthma and was on heparin and venodyne boots for venous thrombo-prophylaxis. His chief presenting complaints improved until day 13, when he had severe pleuritic chest pain with worsening of shortness of breath and was desaturating while breathing ambient air. Computed tomography (CT) of the chest with intravenous contrast revealed aPE involving bilateral upper lobe segmental pulmonary arteries. Given the pattern and timing of thrombocytopenia prior to onset of his symptoms and acute thromboembolism, diagnosis of HIT was made which was later supported by positive platelet factor- ELISA and serotonin release assay (SRA) laboratory testing. Heparin and heparin-related products were promptly discontinued and argatroban was started. Later platelet count increased over 150 × 103/μL and argatroban was switched to warfarin prior to discharge. As heparin is extensively used, all physicians are required to be attentive of this life threatening complication. Discontinuing heparin while substituting with an alternative anticoagulant such as argatroban may become a life-saving strategy in such a case

Sickle Cell Beta-Plus Thalassemia with Subcapsular Hematoma of the Spleen

While splenic complications like hypersplenism, sequestration crisis, and infarction are commonly reported in sickle cell variants like sickle cell beta-plus thalassemia, splenic rupture with hematoma is rare. We present a case of a 32-year-old young male who presented with dull left upper quadrant pain who was found to have multiple subcapsular splenic lacerations and hematoma on abdominal imaging. Hemoglobin electrophoresis confirmed sickle cell beta-plus thalassemia in the patient. There was no history of trauma, and rest of the workup for possible cause of spontaneous rupture of spleen was negative. With the patient refusing splenectomy, he was managed conservatively. Clinicians need to be aware of this rare complication of sickle cell variants

Sickle Cell Beta-Plus Thalassemia with Subcapsular Hematoma of the Spleen

While splenic complications like hypersplenism, sequestration crisis, and infarction are commonly reported in sickle cell variants like sickle cell beta-plus thalassemia, splenic rupture with hematoma is rare. We present a case of a 32-year-old young male who presented with dull left upper quadrant pain who was found to have multiple subcapsular splenic lacerations and hematoma on abdominal imaging. Hemoglobin electrophoresis confirmed sickle cell beta-plus thalassemia in the patient. There was no history of trauma, and rest of the workup for possible cause of spontaneous rupture of spleen was negative. With the patient refusing splenectomy, he was managed conservatively. Clinicians need to be aware of this rare complication of sickle cell variants

Fatal pulmonary cavitary disease secondary to Mycobacterium xenopi in a patient with sarcoidosis

Introduction: Mycobacterium xenopi (M. xenopi) has low pathogenicity and usually requires either host immune impairment or structural lung disease to cause clinical disease. Fatal cavitary infection in a patient without immunosuppression is rarely presented. Case report: A 62-year-old female with history of sarcoidosis and hypertension presented with cough, fever and dyspnea for one week. Chest imaging showed irregular opacification of upper lung zones. The sputum samples tested positive for acid-fast bacilli (AFB) and the subsequent testing identified M. xenopi. She was started on rifampin, isoniazid, pyrazinamide and ethambutol along with azithromycin, and was discharged with plans to continue the same. A follow up sputum test was negative for AFB. She was, however, readmitted ten months later with sepsis due to pneumonia. Chest imaging revealed worsening cavitary lung lesions. Despite starting her on intravenous antibiotics while continuing anti-tubercular therapy, she developed severe respiratory distress and had to be intubated. Her condition continued to deteriorate and she expired the following day. Conclusion: Fatal cavitary infections with M. xenopi have been reported in the absence of established optimal management. Well-designed studies with sufficient power are needed to establish new treatment guidelines

Rare case of Mycobacterium nebraskense presenting as asymptomatic cavitary lung lesion

Introduction: Mycobacterium Nebraskense is a rare nontuberculous mycobacterial infection. The first isolate of the species was from human sputum at University of Nebraska Medical Center. There are only a few cases have been reported and the exact behavior of the disease is not clearly described. Here, we present a case from New York City incidentally found to have a cavitary lung lesion due to M. nebraskense. Case report: An 82-year-old female with a history of diabetes mellitus, hypertension, and dementia presented with constipation and urinary retention for 1 day. She had no fever, cough, shortness of breath, nausea, vomiting, appetite change, or weight loss. Computed tomography (CT) scan of abdomen and pelvis revealed retained fecal material in the colon, non-obstructing left renal calculus, and bilateral small pleural effusion with right-sided lung infiltrates. Subsequent CT scan of the chest showed 4.5 cm pleural-based opacity in right lung base with a small cavity. Sputum smear for Acid-fast bacilli was positive. Mycobacterial culture reported positive growth of M. nebraskense, while polymerase chain reaction returned negative for Mycobacterium gordonae, Mycobacterium kansasii, Mycobacterium avium complex and Mycobacterium tuberculosis. With the patient asymptomatic and her constipation improved, she was discharged with plans for close follow-up as outpatient. Conclusion: M. nebraskense is a very rare nontuberculous mycobacterial infection. From only a few cases reported in the USA, the exact presentation of infection, disease progression, and treatment have not been described well. Asymptomatic cavitary lung disease caused by M. nebraskense has not been reported before

Lung consolidation as a rare presentation of lymphoplasmacytic lymphoma with extramedullary Waldenström’s macroglobulinemia

Objectives: Lymphoplasmacytic lymphoma (LPL) is a mature B cell lymphoma that usually involves the bone marrow, spleen and lymph nodes. Extramedullary involvement, including the lung, is rarely reported. Case description: A 73-year-old female initially presented to our hospital complaining of productive cough of white-colour sputum for three weeks duration. She reported unintentional weight loss of ten pounds over the last five months. There was no history of haemoptysis, fever, night sweats, chills, recent infections or hospitalization. Chest imaging showed right lower lobe consolidation, small right pleural effusion. She was treated with oral antibiotic for pneumonia. After two months, a follow up chest imaging revealed persistent right lower lobe consolidation. Therefore, she was worked up for the possibility of malignancy. Bronchoscopy showed polypoid nodularities surrounded by black discoloured mucosa in the sub-segmental bronchi of the right lower lobe, and biopsy specimen revealed atypical B cell lymphocytic infiltrate. Polymerase chain reaction confirmed a clonal B-cell gene rearrangement supportive for a low-grade B-cell Lymphoma. Subsequently; serum immunofixation showed IgM of 1491 mg/dL (normal range 26–217 mg/dl) with normal levels of IgG and IgA. Urine contained free kappa light chains. Cytology with immunophenotyping of pleural fluid revealed lymphoplasmacytic lymphocytes. This combination of lab and bronchoscopy findings established the diagnosis of extramedullary Waldenström’s macroglobulinemia. Conclusion: Waldenström’s macroglobulinemia, a manifestation of LPL, is associated with an IgM monoclonal gammopathy in the blood. Extramedullary involvement including the lung is rarely seen in LPL. Physicians need to be aware of this rare presentation

Severe hypercalcemia in a patient with extrapulmonary Mycobacterium abscessus: granuloma or immune reconstitution inflammatory syndrome? First case of Mycobacterium abscessus presenting as retroperitoneal lymphadenopathy with severe hypercalcemia: a case report and literature review

Background: Nontuberculous mycobacterium is a recognized cause of hypercalcemia, particularly in patients with acquired immunodeficiency syndrome (AIDS). Here we describe a case of severe hypercalcemia secondary to Mycobacterium abscessus (M. abscessus) in a patient with AIDS. To the best of our knowledge this is the first case report describing a case of M. abscessus presenting as retroperitoneal lymphadenopathy and severe hypercalcemia. Case description: A 56-year-old man with AIDS presented with altered mental status and somnolence for four days. Laboratory investigations were significant for calcium 16.49 mg/dL (RI 8.9–10.3 mg/dL), 1,25 dihydroxyvitamin D level 44.1 pg/ml (RI 19.9–79.3 pg/ml) and parathyroid hormone (PTH) 4 pg/mL (RI 15–65 pg/mL). CT scan of Abdomen and Pelvis showed hepatosplenomegaly with large retroperitoneal, retrocrural, and mesenteric lymphadenopathy which had an intense focal uptake on Gallium scan. Bone marrow biopsy revealed mild plasmacytosis (5%) with no evidence of myelodysplasia, acute leukemia or lymphoma. A subsequent lymph node biopsy showed fragments of fibrous tissue with lymphohistiocytic infiltrate and many acid-fast bacilli. Pre-antibiotic blood cultures grew Mycobacterium which was identified later as M. abscessus at four weeks. Conclusion: hypercalcemia in HIV-infected patients may suggest malignancy or infectious etiology, among other causes. Clinicians should be aware of the risk of hypercalcemia with nontuberculous mycobacterium (NTM) infection, whether as first manifestation or a late presenter in the disease course after initiating antiretroviral therapy (ART). We suggest careful monitoring of serum calcium level upon diagnosis of NTM infection and after initiation of ART, NTM therapy or vitamin D supplementation

Prevalence and Risk Factors for the Development of Abdominal Aortic Calcification Among the US Population: NHANES Study

INTRODUCTION: Abdominal aortic calcification (AAC) is an important marker of subclinical cardiovascular disease and its prognosis. Advanced age, hypertension, smoking, dyslipidemia, diabetes mellitus, and higher truncal fat are known markers of AAC in studies conducted around the world. However, literature for these risk factors and their co-occurrence is limited in the US. MATERIAL AND METHODS: We used data from dual energy X-ray absorptiometry (Hologic, v4.0) to detect the occurrence of AAC in a sample population ( RESULTS: We found the national prevalence of AAC in the US to be 28.8%. After adjusting for confounders, persons with hypertension: OR = 1.66 (95% CI: 1.30-2.13) and smokers: OR = 1.63 (95% CI: 1.24-2.14) were more likely to have AAC compared to their respective counterparts. Increasing age was positively associated with AAC: OR = 1.06 (95% CI: 1.04-1.08). There was a statistically significant negative association between body mass index (BMI) and AAC, more so in smokers than in non-smokers: OR = 0.97 (95% CI: 0.94-0.97). We did not observe any statistically significant association between diabetes and AAC. CONCLUSIONS: Advanced age, smoking, and hypertension was associated with increased occurrence of AAC. Paradoxically, increasing BMI was inversely associated with AAC and there was no statistically significant association between total body and trunk fat percentages and AAC. To the best of our knowledge, this is the first study to establish the nationwide prevalence and associated factors in the US

The Jailed Sinoatrial Node: An Interesting Case of Cardiogenic Shock Secondary to Sinus Arrest Following Percutaneous Intervention

Complete occlusion of the sinoatrial node artery can be a complication of percutaneous intervention (PCI) to the right coronary artery (RCA). When this happens, dysfunction of the sinus node may follow resulting in sinus arrest. When this occurs, it is usually transient and as such, is typically not accompanied by hemodynamic instability. Permanent sinus arrest and shock state may, however, occur on rare occasions. The presence of junctional rhythms on the electrocardiogram (ECG) may predict the occurrence of these permanent arrhythmias and cardiogenic shock. In this case report, we present a 78-year-old woman who developed cardiogenic shock secondary to sinus arrest following PCI to RCA. Her ECG showed junctional rhythm, and she went on to require permanent ventricular pacing. This illustrates a known but rare complication of PCI to RCA