United States

Background
Malaria in the United States is a rare disease with a reported number of cases typically 2,000 each year. In 2022, the State of Ohio had 32 malaria cases: 10 females and 22 males. This mosquito born illness poses a major threat to American travelers, military personnel, and US citizens living abroad in endemic areas. In returning travelers from high-risk countries, Malaria is the most common cause of febrile illness. Plasmodium ovale can remain dormant in the liver and presentation will be delayed. Chronic infection and relapsing disease will persist if the infection is not treated in the initial stages. Relapse episodes may occur months or years later. 

Case Presentation
We present a case of a 39-year-old male with a past medical history of chronic pancreatitis, depression, type 2 diabetes mellitus, gastroesophageal reflux disease, recent Epstein- Barr virus infection, who presents with fever, nausea, and vomiting beginning 10 days prior to admission. The patient has an extensive travel history abroad and returned from Angola six months ago. Prior to admission, he underwent treatment at a different hospital for sepsis, encephalopathy, fever, Epstein-Barr virus and babesia. His condition worsened and he left against medical advice and opted to seek treatment at our facility. With concern for malaria, immediate testing included: Giemsa-stained peripheral blood smear and malaria polymerase chain reaction. His anti-malarial treatment regimen included artemether-lumefantrine tablets for 3 days. Plasmodium species PCR was positive for Plasmodium ovale. The patient responded well to therapy, and continued follow-up at the infectious disease clinic. Likely, the progression and severity of his malaria infection progressively worsened due to delays in treatment and testing. Given his travel history, a concern for malaria should have been on the differential diagnosis at his previous hospital admission.

Discussion
Plasmodium ovale and Plasmodium vivax infection can remain dormant for months and will cause relapses despite anti-malarial prophylaxis treatment. An immunocompromised patient with infection can trigger nonspecific host defense mechanisms. The patient’s symptoms were initially attributed to Epstein-Barr virus infection; unfortunately, there was a missed malaria diagnosis. New research suggests climate change is increasing the mosquito population worldwide and likely causing higher malaria cases. Anti-malarial prophylaxis should be initiated and completed in patients traveling to endemic regions. Returning travelers with flu-like symptoms should be evaluated for malaria as soon as possible.


AMA Research Challenge 2023

A Case of Plasmodium Ovale Malaria Presentation

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Background
Cetuximab is a chimeric antibody used in treatment of metastatic colorectal cancer. Administered via an infusion, the most common side effect of cetuximab is mild allergic response. However, more serious reactions of anaphylaxis and cardiac arrest have been reported. Given the scarcity of the incidence of these reactions, and their reversible nature, there is limited understanding of predisposing factors and essentials of prevention. The present report aims to bridge this gap in knowledge and describes a case of cardiac arrest following cetuximab infusion. 

Case Presentation
A 68-year-old male with a medical history of stage 4 colorectal cancer with metastasis to the lung and liver presented to the emergency department (ED) with cardiac arrest following his first dose of cetuximab as a part of an outpatient clinical trial. Prior to infusion, the patient received 50 mg of Benadryl and underwent an electrocardiogram which revealed no abnormalities. Three minutes following initiation of cetuximab infusion, the patient developed pulseless electrical activity (PEA) and manual cardiopulmonary resuscitation (CPR) was begun. Vitals included a blood pressure of 95/38 mmHg and an oxygen saturation of 73%. En route to the emergency department (ED), the patient was intubated, and manual chest compressions were continued. Upon arrival, Acute Cardiac Life Support protocol was initiated and 2.3 mg of epinephrine was administered. The patient regained cardiac activity after fifteen minutes and was transferred to the critical care unit on an epinephrine drip. 

Initial laboratory testing revealed acidemia with a low bicarbonate level, hyponatremia and hyperchloremia, and normal potassium and magnesium levels. Elevated troponin T levels of (199 ng/L) were observed; however, echocardiography showed no abnormalities except for the slightly prolonged QTC interval in the ECG. Additionally, the patient had a high tryptase level of (63.6 ng/mL), suggesting an anaphylactic response. A CT chest image identified a new large left pneumothorax within a pre-existing subpleural bulla, bilateral rib fractures, and small pleural effusions likely due to recent CPR. The pneumothorax resolved with chest tube insertion. Although the patient initially improved, unfortunately he deteriorated with worsening hypoxia and aspiration pneumonia expired on the eighth day of admission.

Discussion
This case demonstrates the risk of life-threatening acute hypersensitivity responses following chemotherapy infusions, regardless of premedication with antihistamines. It underscores the importance of preliminary allergy testing, close monitoring of electrolytes and tryptase levels during transfusion, and quick access to crash carts.

Cardiac Arrest Following Cetuximab: A Fatal Iatrogenic Outcome

Background:
Coccidioidomycosis, commonly known as Valley Fever, and Paracoccidioidomycosis, referred to as the Mycosis of Lutz, Splendore, and Almeida, are the infections caused by two different types of dimorphic fungi, namely Coccidioides spp and Paracoccidioides spp, respectively, following inhalation of arthroconidia. While the San Joaquin Valley of California and the South-Central region of Arizona are the endemic regions for the Valley Fever, the most paracoccidioidomycosis cases are reported from Brazil, Colombia, Venezuela, and Argentina. The symptoms range from asymptomatic (60% of the total) coccidiomycosis cases to more severe forms, including disseminated infection. Chronic paracoccidioidomycosis comprises over 80 to 90% of total cases and patients with CNS involvement presents with clinical manifestations associated with space- occupying lesions. It is important to note that the disseminated coccidioidomycosis can result in meningitis, a condition if not treated, carries a significant mortality risk of 95% within a span of 2 years. Therefore, early detection plays a pivotal role in ensuring effective management. This article describes a case of disseminated coccidioidomycosis with neuroparacoccidioidomycosis co-infection in an otherwise healthy immunocompetent patient.

Case Presentation:
A 49-year-old Brazilian male presented with an episode of dizziness and near syncope. The head CT scan revealed two brain lesions at left temporal and parietal lobes with surrounding vasogenic edema causing mild mass effect. CT chest showed extensive bilateral small pulmonary nodules and small ill-defined opacities(figure-1), making it indistinguishable from infection due to other infectious, neoplastic, or inflammatory etiologies. Brain MRI revealed two ring-enhancing lesions with perilesional white matter edema. Subsequently, the CSF studies were positive for antibodies to coccidioides TP-antigen and F-antigen, confirming CNS involvement. The fungal isolate from bronchial washing was positive for growth of Paracoccidioides brasiliensis. The patient was treated with Dexamethasone, Fluconazole, and Levetiracetam. The patient is currently receiving the maintenance dose of fluconazole, which is for life.

Discussion:
Chronic paracoccidioidomycosis involving the lung can present as dry cough and dyspnea. The gold standard for diagnosing paracoccidioidomyosis is through isolation of Paracoccidioides spp. in culture and direct myocological examination. CNS involvement with paracoccidioidomycosis has been observed in 10-15 percent of patients presenting with seizures and focal neurologic signs, with positive ring-enhancing lesions with perilesional edema observed in MRI. Disseminated coccidioidomycosis is confirmed by antibody detection in CSF, warranting azole antifungal therapy. For patients with neuroparacoccidioidomycosis, TMP-SMX and amphotericin-B are effective. IV fluconazole is an alternative. Antifungal treatment should be provided to all disseminated coccidioidomycosis patients. To prevent relapse, lifelong antifungal therapy and follow-up are necessary. The role of a single azole for treatment of coexisting coccidioidomycosis and paracoccidioidomycosis infections is still unclear.

Conclusion:
Co-infection of disseminated coccidioidomycosis and paracoccidioidomycosis with neurologic involvement is a rare and unique presentation in a middle-aged otherwise immunocompetent individual. The role of a single azole for the treatment of coexisting coccidioidomycosis and paracoccidioidomycosis infections is still unclear. We aim to add more on literature on the treatment strategies for these disseminated fungal co-infections in the context of lifelong antifungal therapy needed to prevent relapse. Given that there are no proper guidelines for treating disseminated coccidioidomycosis and paracoccidioidomycosis co-infections for longer duration, further studies into the topic are recommended.

Disseminated Coccidioidomycosis with Neuroparacoccidioidomycosis Co-infection: A Rare Case Report and a Literature Review

Background
A post-dural puncture headache (PDPH) is a common complication following trauma from spinal or epidural procedures. While the gold standard of treatment is an epidural blood patch (EBP), numerous pharmaceuticals have been investigated to prevent and manage symptoms with varying results. In some studies, gabapentin has been shown to decrease the incidence and severity of PDPH and opioid consumption without significant adverse effects.
Case Presentation
A 22-year-old female presented with an intractable headache after a recent lumbar puncture (LP). She was receiving treatment with REPOCH and intrathecal (IT) methotrexate for Burkitt’s Lymphoma and had end-stage renal disease status-post a remote kidney transplant complicated by post-transplant lymphoproliferative disorder. At presentation, her associated symptoms included nausea, vomiting, and severe pain that improved with lying flat, consistent with a PDPH. Initial treatment included fluids, opioids, anti-emetics, and caffeine. However, the patient required hospitalization due to her symptoms for which Anesthesiology and Palliative
Medicine were consulted. Since the patient had future cycles of IT chemotherapy and was a high infectious risk due to her immunocompromised state, an EBP was not recommended. Steroids, acetaminophen, and NSAIDs were contraindicated given her neutropenic fever and renal dysfunction, respectively. Gabapentin 100mg TID was then recommended based on limited evidence. The patient experienced significant symptom relief with gabapentin, decreasing her opioid utilization from over 100 oral morphine equivalents to zero within 24 hours. Gabapentin was prescribed for the patient’s future LP schedule that included three days of prophylactic treatment followed by three days of therapeutic treatment. The patient’s last chemotherapy was completed a few months later without recurrence of her headache.
Discussion
Management of PDPH includes a wide variety of treatment options in the literature with new non-opioid medications undergoing ongoing investigation. Clinicians should consider the use of gabapentin in the treatment and prevention of PDPH for patients who fail standard therapies.

The Use of Gabapentin for Relief of Post-Dural Puncture Headache

Brugada syndrome is characterized by coved-type ST-segment elevations in the precordial leads associated with syncope, life-threatening ventricular tachyarrhythmias and sudden cardiac death. When typical ECG findings are present in the absence of symptoms, it is called Brugada pattern. About 25% of cases are associated with loss-of-function mutation of the cardiac sodium channel SCN5A while others may be triggered by drugs with sodium channel-blocking effects, electrolyte abnormalities, febrile states, or autonomic dysfunction.

A 33-year-old man presented with a 3-day history of intermittent substernal chest pressure. On hospital admission, ECG showed normal sinus rhythm without ST-segment changes and serial cardiac enzymes were normal. Given persistent symptoms and unremarkable recent exercise ECG-stress testing, cardiac CT-angiography was performed which revealed anomalous origin of the right coronary artery (RCA) with approximately 50% luminal narrowing. The patient underwent successful surgical reimplantation of the RCA. Cardiopulmonary bypass was weaned
off and the patient rewarmed from therapeutic hypothermia. Once normothermia was achieved, the patient developed ventricular fibrillation (VF). Following successful resuscitation, ECG revealed ST-segment elevations in V1 and V2 consistent with type 1 Brugada, which completely resolved spontaneously in the subsequent hours and was not reproducible with ajmaline challenge.

It is well known that hyperthermia may trigger Brugada syndrome in predisposed individuals. Studies have shown that mutated sodium channels result in temperature-dependent ionic changes. In febrile states, delayed sodium influx results in heterogeneous depolarization predisposing to VF. On the contrary, severe hypothermia (28.5C) causes sinus bradycardia, QT prolongation, widening of the QRS complex and the pathognomonic Osborn wave. Typical Brugada pattern has been rarely described in hypothermic states. Nonetheless, this pattern has been reproduced in animal models with cooling of the epicardium. Therapeutic hypothermia is targeted in the range of mild hypothermia (32-34C), where VF occurs only rarely, mainly in patients with primary arrhythmic disorders. Tan et al. described a case of transient typical Brugada ECG pattern upon rewarming from therapeutic hypothermia after sudden cardiac death of unknown etiology, with complete resolution with normothermia. These authors proposed that the Brugada pattern was hidden during the hypothermic state. In our patient, however, VF occurred only during the rewarming phase when normothermia was
achieved. We hypothesize that temperature increments, not necessarily hyperthermia, may be associated with increased risk of Brugada syndrome in susceptible patients. Although further research is needed, rewarming from therapeutic hypothermia requires careful monitoring for potentially lethal arrhythmogenic disorders.

A Warming Surprise: Brugada Syndrome After Rewarming from Therapeutic
Hypothermia

Background:
The spectrum of vascular access-site complications following cardiac catheterization can vary widely in severity ranging from simple to complex that can contribute to significant morbidity with a high economic burden and healthcare costs.

Aim:
The aim of the case presentation was to describe post-discharge delayed complication (acute limb ischemia) of cardiac catheterization due to noncalcified plaque.

Case Presentation:
A 58-year-old male with a history of coronary artery disease, diabetes mellitus, and hyperlipidemia underwent cardiac catheterization status-post angioplasty to the right coronary artery via right-femoral artery access. The patient was discharged home post-procedure, however, 8 hours later, he developed a sudden-onset cold foot, and worsening numbness, and tingling sensation in his right extremity that prompted him to present to the ER. Physical examination was notable for cold skin in his right leg with diminished dorsalis pedis and popliteal pulses, and a mild loss of “touch sensation” below the level of the knee. The patient was staged “IIa” on the Rutherford Acute Limb Ischemia score. Vitals and labs were within normal limits. CT Angiogram revealed focal high-grade stenosis in the right common femoral artery at the site of a recent arterial puncture from cardiac catheterization. This was likely secondary to nonocclusive, noncalcified plaque that has been disrupted from recent instrumentation. A Heparin drip was initiated and the patient underwent emergent revascularization with a diagnostic angiogram and balloon angioplasty of the right common femoral artery with the placement of a 27mm stent. A completion angiogram showed the resolution of the high-grade stenosis with good flow through the profound and superficial femoral artery. 

Discussion:
The risk of access-site complications following cardiac catheterization, although quite low, is increased with the femoral artery with an incidence estimated to be as high as 17%. Bleeding and hematoma are often reported, however, thrombosis is infrequent with mechanisms involving atherosclerotic plaque rupture or subintimal dissection of the plaque with secondary thrombosis. When the severity of limb ischemia is threatening, immediate anticoagulation followed by surgical revascularization is the most appropriate intervention. Thrombosis at the access site of cardiac catheterization can cause critical limb ischemia, particularly with the femoral artery, thus highlighting the need for careful post-operative follow-up. 


Acute limb ischemia due to iatrogenic plaque rupture in the common femoral artery at the site of cardiac catheterization - A Case Report

An anterior mediastinal teratoma in a child has never previously been reported presenting as a persistent dry cough. In this case, 5-year-old female with an initial history of respiratory syncytial viral infection, presented with a persistent cough for over 2 months. Asthma seemed the likely diagnosis initially. However, chest x-ray showed significant cardiomegaly. Echocardiogram was normal. CT scan of chest showed a large anterior mediastinal mass, likely teratoma. The mass was surgically resected, and diagnosis was confirmed by histopathology. In the future, it is critical physicians perform radiographical imaging to further investigate a persistent cough in pediatric patients.

Anterior Mediastinal Teratoma Presenting as a Persistent Cough in a Child​

Anomalous origin of the left main coronary artery (LMCA) from the right sinus of Valsalva (RSV) is a rare congenital anomaly that can cause myocardial ischemia, ventricular arrhythmia, and sudden cardiac death. We report a case of a 74-year-old male with a history of hyperlipidemia and hypertension who presented with NSTEMI (Non-ST elevation myocardial infarction). On Coronary angiogram patient was found to have LMCA originating from RSV (Image attached) and a 90% stenosis of left anterior descending (LAD) artery. Patient subsequently underwent computed tomography angiography (CTA) to assess the course of the LMCA which was found to be intramyocardial with no compression. Echocardiogram reported reduced ejection fraction (EF) of 40% and wall motion abnormalities in anterior wall. Patient had a successful staged PCI. Patient on follow-up reported no symptoms and EF improved to 50%. Anomalous origin of the LMCA from the RSV is a rare but potentially life-threatening congenital anomaly Further research is needed to determine the optimal treatment for this anomaly and to improve the long-term outcomes of affected individuals.

Acute Coronary Syndrome (ACS) and Anomalous Left Main Coronary Artery: A Case Report

Hepatitis C virus (HCV) has a predisposition to spread via lymphatic route to extrahepatic sites. One common site is the heart. About 17–37% of HCV-infected individuals experience cardiac problems like cardiomyopathies, myocarditis, atherosclerosis, CVA's (stroke and ischemic heart disease), and coronary and peripheral artery disease. There are various mechanisms through which HCV can cause cardiomyopathies, however, in rare instances, the resultant dilated cardiomyopathy follows a transient course. Patients with early initiation of antiviral treatment and achievement of sustained virologic response(SVR) are seen to have reduced risk and better prognosis for HCV-related cardiovascular abnormalities. We report a case of a 65-year-old male with a history of congestive heart failure, atrial fibrillation, and a chronic HCV infection who presented to the hospital with worsening shortness of breath, lower leg swelling, and a six-month history of progressive dyspnea on exertion and fatigue. Initial echocardiography revealed severe left ventricular dysfunction with an EF of 25%. Cardiac magnetic resonance imaging (MRI) confirmed the presence of cardiomyopathy but did not reveal any evidence of myocardial infarction or ischemia. After managing the patients with appropriate antiviral therapy (sofosbuvir and ledipasvir) and adequate treatment for heart failure, we noticed a significant clinical improvement in the patient's heart failure symptoms and a 20% rise in his ejection fraction. Then we review the present literature about transient dilated cardiomyopathy in patients with chronic HCV infection, as well as describe our experience in diagnosis and management of this unusual complication.

Hepatitis C virus (HCV) has a lymphotropic nature, leading to its spread to extrahepatic sites, including the heart. Cardiac problems, such as cardiomyopathies, myocarditis, atherosclerosis, stroke, ischemic heart disease, and coronary/peripheral artery disease, occur in approximately 17-37% of HCV-infected individuals. HCV can contribute to cardiomyopathies through various mechanisms. However, in rare cases, resulting dilated cardiomyopathy may follow a transient course. Early initiation of antiviral treatment and achieving sustained virologic response (SVR) has been associated with reduced risk and improved prognosis for HCV-related cardiovascular abnormalities.

HEPATITIS C VIRUS AND CARDIAC HEALTH: IDENTIFYING DILATED CARDIOMYOPATHY, TREATMENT AND CLINICAL OUTCOMES

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