United States

Background:
Dog bites are a well-known mode of transmission for Capnocytophaga canimorsus. However, patients rarely present with meningitis. The few reported individuals experience high fevers and have concerning rates of neurological sequelae upon recovery. Common risk factors include a compromised immune system, alcoholism, and animal exposure. Although most patients recover with sufficient antibiotic treatment, the selected course varies widely. Here, we present an unusual case of brain infarction and subarachnoid hemorrhage in addition to Capnocytophaga canimorsus meningitis.

Case Presentation:
A 74-year-old man with history of seizures, hypertension, and smoking presented to our hospital with a one-day history of malaise and after being found unresponsive by his wife. Upon arrival to the hospital, he was found to have seizures, a high fever of 39.1°C, and hypoxemia requiring 4 L of oxygen via nasal cannula. The patient received levetiracetam, ceftriaxone, and vancomycin. Lumbar puncture was performed and yielded cloudy cerebrospinal fluid (CSF) with a WBC count of 1185 cells/mm3 (98% polymorphonuclears), glucose of 9 mg/dL, and protein of 417 mg/dL. Gram stain revealed gram-negative bacilli, and the culture showed Capnocytophaga canimorsus susceptible to ceftriaxone (MIC 0.25), with low MICs for ciprofloxacin, meropenem, and penicillin. Brain MRI showed multiple embolic infarcts and subarachnoid hemorrhage. Transthoracic echocardiogram showed no vegetations. The patient was treated with 4 weeks of intravenous ceftriaxone and clinical follow up showed clinical improvement after antibiotic treatment.

Discussion:
In the case presented, this individual required longer antibiotic treatment than the reported median of 15 days. Of the three prior reported cases with acute brain infarction during infection, two had lingering neurological issues and also required bilateral lower extremity amputation. A hyperinflammatory state, vasospasm, and activation of the coagulation cascade have all been hypothesized to contribute to the association between bacterial meningitis and cerebral infarction. This known complication in meningitis has severe repercussions for the long-term recovery of patients. Prompt recognition and treatment is vital to limb salvage and optimal neurological recovery.

AMA Research Challenge 2024 

A rare case of Capnocytophaga canimorsus meningitis with acute cerebral infarct and subarachnoid hemorrhage

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Introduction:
Klebsiella pneumoniae is a well-described etiology of pyogenic liver abscess (PLA) in patients from Southeast Asia, but rarely outside of that region. We present a rare case of Klebsiella PLA in Eastern Long Island in a patient with no travel history to Southeast Asia.

Case Presentation:
A 71-year-old Puerto Rican male with PMH diabetes, hepatitis C s/p treatment presented with dull, non-radiating right lower quadrant pain associated with non-bloody non-bilious vomiting and intermittent fevers for 2 weeks. He denied other previous gastric or hepatobiliary disease or malignancy, abdominal trauma/surgeries, alcohol use, IV drug use, history of pancreatitis or liver transplant, PPI use, or any travel history in the last 15 years. On examination, T 102.8°F, BP 126/86, HR 96, RR 27, SpO2 99% on RA; he had tenderness in the right lower quadrant. Labs showed normal WBC and hepatic function, and mildly elevated alkaline phosphatase at 142. CT abdomen/pelvis with oral and IV contrast showed a liver mass (Figure 1). Subsequent MRI abdomen with and without IV contrast (Figure 2) demonstrated a 6.1 x 6.9 x 6.9 cm posterior right hepatic lobe abscess. He was admitted for sepsis secondary to liver abscess and started on broad-spectrum antibiotics. The abscess was drained and fluid culture subsequently grew Klebsiella pneumoniae. The patient improved clinically during the remainder of the hospitalization and was discharged on four weeks of oral levofloxacin.

Discussion:
Pyogenic liver abscesses (PLA) are pus-filled masses that can develop after hematogenous spread from an intraabdominal infection, bacteremia, or nearby liver injury. The incidence of pyogenic liver abscess is about 2.3 cases per 100,000 people and has been well-described in Southeast Asia – especially in Taiwan. Klebsiella pneumoniae PLA has been reported in Taiwan since the 1980’s with more than 900 cases identified, as compared to only 50 cases in Western countries from the 1990’s to early 2000s. In another extensive literature review, only 93 cases were found in the United States from 1949 to 2016. 80% of PLA cases found Klebsiella pneumoniae as the predominant bacteria, as compared to non-Eastern Asian countries, where E. coli and Streptococcus species predominate. Risk factors include diabetes, history of hepatobiliary infection or colorectal cancer, abdominal trauma or surgeries. Clinical features include fever, right upper abdominal, nausea and vomiting. Labs may show leukocytosis, hyperbilirubinemia, elevated ALP/ AST. MRI with IV contrast is the most sensitive study. Treatment involves drainage and antibiotic therapy, with good prognosis.

Conclusion:
Clinicians should keep rare etiologies in mind for patients who present with liver abscesses.


But I Never Went to Southeast Asia! A Rare Case of Klebsiella penumoniae Pyogenic Liver Abscess in Eastern Long Island

Fournier's gangrene (FG) is an uncommon and life-threatening necrotizing fasciitis affecting the perineum and genital region. This condition typically involves polymicrobial infection of the deep soft tissues and fascial planes. FG occurs more frequently in diabetic patients due to impaired immune function, hyperglycemia, microvascular complications, peripheral neuropathy, or genital and urinary infections. In this case, it is observed that it can also develop in a non-diabetic individual, presenting a considerable diagnostic and treatment challenge.

Fournier’s Gangrene in a Non-Diabetic Female Presenting with Severe Hypoglycemia: A Case Report

Introduction
Early administration of intramuscular epinephrine can be life-saving in the acute management of anaphylaxis. Rarely, intracranial hemorrhage (ICH) can occur after epinephrine use due to rapid elevations in blood pressure. We report a rare case of a man who developed ICH following epinephrine injection for acute anaphylaxis.
Case Description
A 70-year-old man with end-stage renal disease on dialysis, hypertension, and diabetes presented to the emergency department with a 1-month history of left ear pain. He had no prior history of anaphylaxis, intracranial hemorrhage, stroke, or allergies. Initial vital signs showed blood pressure of 203/87 mmHg. Physical exam revealed left edematous ear canal and mastoid tenderness, with no focal neurologic deficits. Suspected mastoid infection prompted a CT temporal bone scan with contrast, which was consistent with otomastoiditis and showed no evidence of intracranial hemorrhage or other intracranial pathology. Empiric antibiotic treatment was given with cefepime and vancomycin. Within 10 minutes of initiating vancomycin infusion, he developed shortness of breath and tongue/facial swelling, with blood pressure 152/116 mmHg. The patient then rapidly decompensated, developing altered mental status, bradycardia (30 bpm), hypoxia (40% O2 on pulse oximetry), and minimally palpable pulse. Anaphylaxis was suspected, and 0.3 mg intramuscular epinephrine, diphenhydramine, and dexamethasone were given. A repeat BP 5 minutes later showed hypertension up to 261/102 mmHg. Due to altered mental status and for airway protection, an emergent surgical airway was established with subsequent blood pressure 114/108 mmHg twenty minutes after sedation and ventilation with tracheostomy tube. Patient was subsequently admitted to the intensive care unit. Four days later, MRI brain with/without contrast for evaluation of osteomyelitis showed incidental bilateral intraventricular hemorrhage and acute pontine hemorrhages, confirmed stable by subsequent CT six hours later. Patient had no neurologic deficits and was discharged to a rehabilitation facility 35 days later with a tracheostomy collar.
Discussion
First-line treatment of anaphylactic shock is administration of epinephrine; however, adverse events can occur. Epinephrine can cause short term elevations in systolic blood pressure. Factors that can cause precipitation of intracranial hemorrhage include platelet dysfunction in the setting of chronic kidney disease with dialysis and hypertensive urgency. Physicians should be aware of ICH as a rare cerebrovascular complication of epinephrine injection in the setting of anaphylaxis, particularly in elderly patients with hypertension and high bleeding risk.

Intracranial Hemorrhage Following Epinephrine Injection for Anaphylactic Shock: A Rare Complication 



Abstract Title:
Navigating Anaplasmosis: A Case Report Highlighting Diagnosis and Treatment
Background:
Human Granulocytic Anaplasmosis caused by Anaplasma phagocytophilum is an emerging concern in the United States, spread by Ixodes scapularis and Ixodes pacificus in the Northeastern and Midwestern regions and in the Western regions, respectively. Tick-borne infections are increasingly reported during the summer months, especially in Pennsylvania. Lyme disease remains the most reported tick-borne illness in the state. Anaplasmosis presents unique challenges due to its nonspecific clinical manifestations and potential to mimic other tick-borne diseases. Preventing tick bites prevents the spread of infections.
Case Presentation:
The case of a 68-year-old male patient highlights the critical importance of recognizing and diagnosing anaplasmosis promptly. He presented to the ED with sudden onset high-grade fevers at 103°F, chills, abdominal pain with nausea and vomiting, and generalized weakness. His heart rate was 105/min and BP was 146/87 mm Hg. Fever panel was negative. With alarming findings such as profound thrombocytopenia (platelets decreasing from 102 K/mcL to 56 K/mcL within a day), transaminitis, and elevated CRP levels at 322.1 mg/dL, admission for suspected sepsis of unclear origin was necessitated. Empirical treatment with IV Doxycycline, Atovaquone, and Azithromycin was initiated to cover potential tick-borne infections. Radiological investigations, including CT scans and echocardiography, were unremarkable, further complicating the diagnostic process. The patient's history of living in wooded areas, owning dogs, and previous deer rearing raised suspicion for a tick-borne illness, despite no recollection of a recent tick bite. Definitive diagnosis was achieved through a tick-borne PCR panel, which confirmed Anaplasma phagocytophilum infection. This gram-negative intracellular bacterium selectively infects neutrophils, leading to the characteristic intracytoplasmic inclusions known as morulae, observed on peripheral blood smear. Given the patient's old age, he was at increased risk for severe complications such as systemic inflammatory response syndrome and multiorgan failure. Following a five-day course of IV Doxycycline, the patient's clinical status improved with resolution of fever and thrombocytopenia. He was discharged on oral Doxycycline and Atovaquone, emphasizing the importance of timely intervention and appropriate antimicrobial therapy in managing anaplasmosis.
Discussion:
This case underscores the challenges in diagnosing tick-borne illnesses, particularly in non-endemic regions with limited awareness. Heightened clinical suspicion due to drastic thrombocytopenia, prompt empirical treatment, and utilization of specific diagnostic tools such as NAAT/Tick-borne PCR panels are crucial in achieving favorable patient outcomes. Early recognition of clinically compatible symptoms associated with thrombocytopenia remains paramount in combating the rising incidence of tick-borne infections across the United States.



Navigating Anaplasmosis: A Case Report Highlighting Diagnosis and Treatment

Background 

Patients with Limb Girdle Muscular Dystrophy (LGMD) and other RYR1 variants present unique challenges to the anesthesiologist because of muscle weakness and potential for malignant hyperthermia (MH). We describe the anesthetic management of a patient with LGMD and a potentially difficult airway. 

Case Presentation 

A 55-year-old male with LGMD and no prior exposure to anesthesia presented for resection of colon cancer. The patient’s LGMD predominantly affected his shoulders. Pre-anesthesia examination and routine blood tests were within normal limits. While LGMD is not associated with difficult airways, there was concern for one because of the patient’s small mouth opening and beak-shaped mouth and jaw. Thus, an awake-fiberoptic intubation was performed and the airway was secured with a 7.0 mm endotracheal tube. The anesthesia team took precautions for MH and used a new anesthesia machine to avoid triggers. In the operating room, the patient was positioned at 45 degrees and semi-reclined. Maintenance of anesthesia was achieved with total intravenous anesthesia (TIVA) with propofol, dexmedetomidine, fentanyl, and paralysis with rocuronium. The patient was managed conservatively in the postoperative period and extubated without incident the following day. 

Discussion 

Literature on safe anesthetic management of LGMD is limited. In this case report, we highlight the successful use of TIVA in avoiding MH triggers, and the use of awake-fiberoptic intubation as an effective technique for securing a difficult airway in a patient with LGMD. 
Inhaled anesthetics and succinylcholine are contraindicated in LGMD patients because of an increased risk of developing MH, rhabdomyolysis, and hyperkalemia [1]. Using TIVA avoids the triggers of MH while maintaining appropriate anesthetic depth. Interval measurement of lactate and CK are also important in monitoring for development of MH. Dantrolene should be readily available for suspected MH. 
LGMD increases the risk of respiratory compromise under anesthesia, particularly since muscle relaxants can further exacerbate existing respiratory weakness. Awake-fiberoptic intubation requires thorough pre-anesthesia airway assessment and planning, preserves spontaneous ventilation, and mitigates the risk of respiratory decompensation associated with muscle relaxation, allowing for a controlled and gradual approach to securing the airway. In this case, a thorough airway assessment revealed potential challenges (limited mouth opening, and beak-shaped mouth and jaw) that could have complicated conventional intubation. Anticipation of potential airway challenges and advanced planning for an awake-fiberoptic intubation ensured a safe intubation and successful anesthetic for this patient.

Anesthetic Challenges of a Patient with Limb Girdle Muscular Dystrophy

Although uncommon, the loss of artificial valve components during surgery has been documented in the literature. If a valve fracture occurs intraoperatively, parts of the valve can either remain within the heart cavities or migrate distally into the thoracoabdominal aorta or aortic bifurcation. When the disc fragments, it may be found in the iliac, femoral, or even popliteal arteries. Historically, computed tomography (CT) scans have proven more effective in locating these fragments compared to plain radiography, angiography, and ultrasound.

Missing Aortic Valve Leaflet in Double Valve Replacement Surgery

Background
Pacemaker implantation is routine in modern day medicine, with nearly one million performed annually worldwide, and 200,000 in the United States alone. Despite being so commonplace, cardiac device implant can be associated with serious complications which require awareness for prevention and appropriate treatment. We present an unusual case of pneumomediastinum, pneumopericardium and contralateral pneumothorax following pacemaker implantation.

Case Presentation
A 71-year-old male with a history of coronary artery disease requiring multiple stents, ischemic cardiomyopathy causing heart failure with mildly reduced ejection fraction (40-45%), abdominal aortic aneurysm requiring endovascular aorta repair, hypertension, type II diabetes, and atrial fibrillation presented to the hospital after a significant conversion pause was noted by event monitoring. He subsequently underwent dual chamber pacemaker placement via the left subclavian vein with creation of a left chest wall pocket; insertion of the ventricular lead in the left bundle branch area was noted to be challenging requiring multiple attempts. However, the dual chamber pacemaker implantation was otherwise routine without immediate complications. Proper lead position was confirmed via fluoroscopy.

The patient was admitted overnight for observation. The following morning, routine chest x-ray discovered a right apical pneumothorax and pneumomediastinum. Subsequent CT chest revealed moderate-volume right pneumothorax and pneumopericardium, with the atrial lead extending into the right pleural space. The right atrial lead tip bored through the atrium into the lungs, creating a channel leading to communication between lung parenchyma, pleural space and the pericardium. The surgery service subsequently placed a right-sided chest tube. Imaging the next day demonstrated resolution of pneumothorax and pneumopericardium. The chest tube was removed the following morning, with the patient remaining asymptomatic throughout his post-procedural recovery. Due to concern for potential dislodgement or further extension of the right atrial lead into the right pleural space, it was successfully extracted prior to discharge. 

Discussion
This case represents an unusual mechanism of pneumothorax after pacemaker implant, which typically occurs due to inadvertent lung puncture ipsilateral with vascular access. Patients with pneumothorax and pneumopericardium may initially present asymptomatically, then later develop symptoms days later including pleuritic chest pain and shortness of breath. Findings may not be readily apparent on chest x-ray depending on burden of air and may require lead removal or repositioning. Clinicians must maintain a high index of suspicion when thoroughly analyzing post-procedural images.

A Lighthearted Case: Pneumopericardium and Contralateral Pneumothorax following Pacemaker Implantation

Background:
Lyme disease is the most common tick-borne illness in the United States, with a prevalence of approximately 500,000 cases annually. Myocarditis is a rare Lyme complications recent data demonstrated prevalence of Lyme myocarditis to be 1% and usually appears 1-2 months after initial infection. We hereby present a rare case of early-onset Lyme Myocarditis.

Case Presentation: 
A 35-year-old male with no significant past medical history presented to the hospital with four days of fever, myalgia, and headache. The day prior to admission, he found a tick at his home and developed a circular rash. He denies chest pain, SOB, palpitations, dizziness. He had no prior medical or family history of cardiac disease and denied tobacco, alcohol, and illicit drug use. He lives with his wife and owns a dog. On physical examination, T 102.6F, HR 103, BP 109/68, RR 19, SpO2 96% on room air. A target lesion was noted on his right thigh; rest of the physical examination was benign. His labs revealed positive serology for B. Burgdorferi IgM antibody, positive western blot, high sensitivity troponin 240; EKG was normal sinus rhythm with no ST or T wave changes. The patient was diagnosed with early localized Lyme disease and discharged home on doxycycline; the troponin elevation was attributed to the fever. He returned to the hospital the next day with chest pain and palpitations; exam was normal, high sensitivity troponin was 267 and ECG was unchanged. Echocardiogram demonstrated EF of 60% without any valvular abnormalities or effusions. He declined cardiac catheterization; a pharmacological nuclear stress test did not show perfusion defects. He was diagnosed with Lyme myocarditis and treated with two-weeks course of ceftriaxone with clinical improvement. 

Discussion: 
Myocardial involvement in Lyme disease results from spirochete colonization in cardiac tissue and subsequent exaggerated immune response, most commonly leading to myocarditis and subsequent heart block; which occurs 1-2 months after Borrelia infection. Typical clinical manifestations of Lyme myocarditis include palpitations, chest pain, conduction abnormalities, pericarditis and heart failure. The diagnosis is clinical and made by, positive Lyme serology accompanied by EKG changes and symptoms. other tests that can point to cardiac involvement include troponins, positive echocardiogram, and negative CAD testing. Treatment depends on clinical status; asymptomatic patients with 1° AV block can be treated with oral antibiotics, whereas symptomatic patients will require IV antibiotics, and patients with 3° heart block may require temporary pacemakers. 


A rare-case of early stage lyme myocarditis

Background: The incidence of gastro-intestinal stromal tumors is 1-2% of all gastrointestinal malignancies [1]. These rarely metastasize to the heart [2], causing atrial fibrillation. The drug of choice is imatinib. This is known to have GI side effects, and infrequently, direct cardiac toxicity. Here, we present a case of atrial fibrillation in a patient with GIST on imatinib therapy, and outline the workup of this rare presentation. 
Case: 84 year old male with spindle cell GIST (4.9 X 3.5 cm) in the gastric fundus, on imatinib 400mg OD for 3 weeks was hospitalized for new onset atrial fibrillation (Figure 1), fever and lymphadenopathy. No history of shortness of breath, chest pain, headaches or palpitations. There is history of severe diarrhea, vomiting and weakness in the last week.  On examination, vitals were normal. Bloodwork showed an eosinophil manual count of 73% (normal: <7%) and atypical lymphocytosis. Workup for the cause of atrial fibrillation (echo, cardiac CT, chest X ray, electrolytes) was done and was normal. Patient was started on eliquis 2.5 mg BD and rate control for atrial fibrillation. Patient developed AKI and transaminitis during the course of hospitalization. Imatinib was held, and patient was started on steroids. On steroids, his eosinophil count normalized, rhythm returned to sinus, renal and liver function dropped back to baseline. The patient was referred to oncology to switch to a different tyrosine kinase inhibitor. Steroids were tapered and discontinued. Patient was asked to review in cardiology clinic for follow – up of atrial fibrillation. 
Discussion: Four potential causes of AF were considered in this patient: cardiac metastasis from the GIST, direct drug toxicity, dehydration induced, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) syndrome due to imatinib [3,4]. Imaging revealed no evidence of cardiac metastasis. Electrolytes were normal, ruling out dehydration as a cause. AF is an uncommon side effect of imatinib (0.55% of patients) [5]. In this case, temporal correlation suggested a possible association. However, the markedly elevated eosinophil count raised suspicion for DRESS [6]. Scoring according to RegiSCAR system suggested probable DRESS. The patient markedly improved on steroids, further confirming our theory. Several studies have reported cases of imatinib-induced DRESS syndrome, and atrial fibrillation in DRESS (7.1%) [3] supporting our clinical findings.  In conclusion, this case is a good example of the importance of considering multiple etiologies for AF in cancer patients undergoing targeted therapy. Clinicians should remain vigilant, follow a comprehensive diagnostic approach and promptly intervene to mitigate adverse events. 

Atrial Fibrillation in a Patient with GIST on Imatinib – What are the causes?

Background: 
Pulmonary embolism (PE) is a life-threatening condition characterized by the blockage of a pulmonary artery or one of its branches. The intricate relationship between substance abuse and thromboembolic events has emerged as a significant concern in clinical medicine. Cocaine, a potent vasoconstrictor, has been associated with both arterial and venous thrombotic events due to its prothrombotic effects on the coagulation cascade and its impact on the vascular endothelium. We present a case of a 42-year-old male with a history of cocaine abuse who presented with a life-threatening PE. 
Case Presentation: 
A 42-year-old male with a past medical history of cocaine abuse presented after a syncopal episode. He described the episode as passing out from a standing position and regaining consciousness quickly on the ground. He endorsed a 3 day history of worsening dyspnea and lightheadedness. On examination, the patient was experiencing mild respiratory distress and was found to be tachycardic. ECG revealed sinus tachycardia with evidence concerning for right heart strain. Laboratory findings were significant for elevated troponin and pro-BNP. 
A ventilation/perfusion lung scan was ordered which showed a high probability of PE. A subsequent CT angiography of the chest was performed which confirmed acute bilateral pulmonary emboli with moderate-large clot burden and evidence of right heart strain with a right ventricle to left ventricle size ratio of 1.35. Lower extremity doppler ultrasound was positive for deep vein thrombosis in the right popliteal vein. 
The patient was evaluated by the interventional cardiology team and was taken for mechanical thrombectomy of the pulmonary emboli. Pre-intervention right heart catheterization was significant for a mean pulmonary artery pressure of 47 mmHg and a pulmonary capillary wedge pressure of 23 mmHg. The clot burden was reduced by greater than 90% and excellent filling with a good venous phase of all pulmonary arteries was noted. The patient improved symptomatically after the procedure. 
Discussion: 
Cocaine's prothrombotic properties are multifaceted, involving the activation of the coagulation process and the secretion of von Willebrand factor (VWF), among other factors, which collectively contribute to thrombus formation. The presence of adulterants in cocaine, such as levamisole, further complicates its pathophysiological impact, potentially exacerbating pulmonary damage and fibrosis, thus predisposing individuals to thromboembolic events. The reported case emphasizes the need for a high index of suspicion for cocaine-induced PE in patients with a history of substance abuse presenting with symptoms suggestive of thromboembolic events.

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