United States

These Antibiotics Just Aren’t Working: Fever of Unknown Origin and an Uncommon Culprit

Kajol Patel MD, WellStar MCG Health Department of Neurology; Nicholas Fuchs BBA Medical College of Georgia; Alexander Warner MD, WellStar MCG Health Department of Internal Medicine; Derek Backer MD MPH, WellStar MCG Health Department of Internal Medicine

Background: Fever of unknown origin (FUO) is defined as a periodic temperature of at least 38.4°C lasting longer than 3 weeks, with a diagnosis remaining uncertain after 1 week of evaluation. The potential etiologies of FUO are diverse, which adds to the challenge of determining the cause. We report a case of FUO that ultimately led to the diagnosis of a very rare cause of fever in adults: Adult-onset Still’s disease (AOSD). Cases like this pose a diagnostic dilemma due to the hesitancy to withhold antimicrobials in the presence of a persistent fever. However, despite the lack of an accepted standard workup for FUO, a thorough and methodical evaluation increases the likelihood of arriving at a treatable diagnosis.

Case Description: A 41-year-old female with a past medical history of psoriatic arthritis presented to the hospital after more than 2 weeks of undulating fevers and bilateral leg pain. She has a past history of psoriatic arthritis and a remote history of IV drug use reportedly in remission. She had previously been treated with antibiotics but no source was clearly identified. Her review of systems included pertinent positives such as odynophagia, salmon colored rash which worsened with the fevers, polyarthralgia, and negatives such as lack of cough or shortness of breath, diarrhea, or dysuria. She had a neutrophilic leukocytosis, markedly elevated CRP and ESR, and markedly elevated ferritin. After ruling out alternatives such as bacteremia, endocarditis, occult abscess, thrombosis or other connective tissue diseases, it was noted that the patient fulfilled 3 major and 4 minor Yamaguchi criteria and the diagnosis of Adult-onset Still’s Disease was made.

Case Discussion: Adult-onset Still’s disease is a very rare cause of fever of unknown origin. Its symptoms include inflammatory arthralgia, a salmon-colored rash, sore throat, lymphadenopathy, and hepatosplenomegaly. AOSD is estimated to occur in 0.16-0.4 per 100,000 persons. Due to its rarity and symptom overlap with other conditions, diagnosing AOSD can often take several months.
This case highlights AOSD as a rare but debilitating cause of FUO. If left untreated, AOSD can lead to significant morbidity and irreversible organ damage. Our case demonstrates the importance of conducting an exhaustive evaluation for alternative causes of FUO before initiating steroids or disease-modifying antirheumatic drugs. When the correct therapy is initiated, the response can be both dramatic and rewarding.

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These Antibiotics Just Aren&#39;t Working: Fever of Unknown Origin and an Uncommon Culprit


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These Antibiotics Just Aren't Working: Fever of Unknown Origin and an Uncommon Culprit


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Background:
Cameron lesions refer to linear ulcers or erosions found on the crests of mucosal folds near the diaphragmatic impression in individuals with significant hiatal hernias. Bleeding from this lesion can cause significant iron deficiency anemia (IDA). Here, I will discuss a case report of an elderly woman who presented with syncope and later was found to have IDA due to Cameron’s lesion associated with large hiatal hernia.
Case Presentation:
An 86 years old, Caucasian female with the history of HTN, meningioma, CVA, seizure presented to the ER with sudden loss of consciousness. During extensive diagnostic workup at ER, she was found alert, oriented to time and place with normal physical and systemic examination. Her laboratory report showed a Hb level of 10.8g/dL with a hematocrit count of 30.1%. CT scan of head without contrast was normal. Chest X-ray showed no acute abnormality except the presence of a large hiatal hernia.
As she has a history of seizure disorder and her anti-epileptic medication was at subtherapeutic range (Dilantin 4.5), a neurologic consultation was requested. Therefore, she underwent an EEG, and it showed normal findings. Unfortunately, she became weak over the following day and her blood report showed a significant drop in Hb% (Hb 7.3g/dL). Hence, she was scheduled for an urgent upper GI endoscopy.
EGD report showed normal hypopharyngeal apparatus with normal esophagus though there was some tortuosity in distal aspect. Partially intrathoracic stomach (35cm-46cm) was noted with retroflexed view of fundus and cardia. A Cameron’s lesion was found along the mucosal folds of gastric fundus. No active bleeding was found. She was diagnosed with hiatal hernia (11cm) with Cameron’s lesion. The patient was discharged with PPI, oral iron tablet, with her regular medications. On her follow up appointments, she showed excellent response to PPI and her Hb% improved with the treatment.
Discussion:
Cameron lesions may go unnoticed and might be less frequently reported due to the need for a keen sense of suspicion for diagnosis, familiarity with endoscopic visuals, and a thorough examination of the hiatus hernia (HH). Cameron lesions have been reported in up to 5% of patients with HH and up to 13.7% of patients with a large HH (>5cm). This 86 years old lady had a large silent hiatal hernia without any gastric reflux symptoms that ultimately resulted in the development of Cameron’s lesion and subsequent bleeding of the lesion led to the development of IDA.


Unveiling the Mystery: Exploring Syncope in an Elderly Woman and the Discovery of Cameron's Lesion in the Stomach with a Large, Silent Hiatal Hernia: A Case Report

Background
Lacunar infarcts are a type of ischemic stroke caused by the occlusion of small penetrating arteries that supply the subcortical deep brain structures such as the basal ganglia, thalamus, white matter of the internal capsule and pons. These arteries are susceptible to blockages due to conditions like hypertension and diabetes. Typical lacunar syndromes include pure motor hemiparesis, pure sensory, ataxic-hemiparesis, dysarthria-clumsy hand and sensory motor with minimal cortical findings. An atypical lacunar infarct can affect non-traditional brain regions and therefore present with unusual symptoms, challenging diagnosis and requiring careful consideration in clinical evaluation and management strategies.

Case Presentation
A 75-year-old male with no significant past medical history presented to the ED with visual changes and dizziness that began a day prior. He reported lateral and downward deviation of the right eye and difficulty ambulating due to dizziness. In the ED, his blood pressure was 230/19 mmHg. Administration of amlodipine 5 mg was unsuccessful in reducing his blood pressure. A CT head with and without contrast, and a CTA of the head and neck, ruled out acute processes. Ophthalmology's differential included neurological causes involving the optic pathway to the lateral geniculate and conditions such as glaucoma. Neurology noted possible 3rd nerve involvement and ataxia, indicating the need to rule out a brainstem lesion. Significant adduction issues of the left eye and a positive Romberg’s sign were also observed. An MRI performed 3 days later revealed an acute lacunar infarct in the dorsal pons affecting the medial longitudinal fasciculus, alongside a mild burden of chronic small vessel ischemic changes in the periventricular and deep cerebral white matter and pons. 

Discussion 
In the presented case, the patient's symptoms of visual changes, dizziness, and neurological deficits, initially perplexing with normal CT and CTA findings, ultimately led to the discovery of an atypical lacunar infarct in the dorsal pons. The involvement of the medial longitudinal fasciculus (MLF) explains the patient's distinctive clinical features, including lateral and downward deviation of the right eye, ataxia, and third nerve palsy. These findings underscore the variability in lacunar infarct presentations, necessitating a high index of suspicion and comprehensive evaluation, especially when initial imaging studies are inconclusive. Chronic small vessel ischemic changes observed on MRI highlight the cumulative vascular burden in the brain, suggesting a predisposing condition for the acute lacunar event. Management involves controlling vascular risk factors to prevent further infarcts and addressing specific neurological deficits through targeted therapies and rehabilitation. This case emphasizes the importance of detailed clinical assessment, multimodal imaging, and specialist consultation in unraveling atypical lacunar infarcts, ensuring appropriate diagnosis and management for optimal patient outcomes.




Unveiling the Unusual: A Case of Atypical Lacunar Infarct in a 75 year old male

Background
Scurvy is thought to be a malady of the past; however, cases still arise in modern populations susceptible to vitamin deficiencies. Vitamin C deficiency notoriously presents as easy bruising, gingivitis, arthralgias, and corkscrew hair. Instead, this disease can mimic signs of vasculitis, which may lead to a delay of diagnosis. For instance, pulmonary arterial hypertension (PAH) is a rare complication of vasculitis, thought to arise from direct involvement of the pulmonary vasculature. To the present authors’ knowledge, the development of PAH in a case of scurvy has not been reported in modern publications. Here we present a case of scurvy in a young adult who presented with symptoms of vasculitis and associated PAH.
Case Presentation
A 30-year-old male with no medical history living in a major metropolitan city presents with myalgias, weakness, petechiae and profound shortness of breath. He has a history of heavy alcohol use in the months prior to admission but recently quit. He reports no drug use or recent bariatric surgery. On presentation, his vitals were stable. On examination, he has non-palpable red-purplish, reticular-appearing discoloration of skin in LE. Lab findings and peripheral blood smear showed macrocytic normochromic anemia with slight anisocytosis. Echocardiogram showed evidence of PAH with dilated right atrium and ventricle associated with elevated RVSP.
There was concern for systemic vasculitis, but the laboratory workup, skin biopsy and immunofluorescence were negative. Urinalysis was positive for bilirubin and urobilinogen but negative for protein and casts. There was no improvement after Prednisone for 7 days. Due to the patients history of heavy alcohol use and negative vasculitis workup we requested a Vitamin C level which was undetectable. After supplementation, there was complete resolution of all symptoms. Hemoglobin returned to normal limits and PAH resolved.
Discussion
This case highlights vasculitis with signs of PAH as a rare representation of scurvy. The similarity poses a diagnostic challenge for healthcare providers as vitamin deficiencies are uncommon in major metropolitan cities. When confronted by a patient who is susceptible to vitamin deficiencies - such as those with a history of heavy alcohol use, nutritionally restricted diets, or psychiatric illness - physicians should not discount the diagnosis of Scurvy. By documenting this case, we hope to provide physicians with evidence to support the possibility of vitamin C deficiency during vasculitis workup.

Vitamin Sea: An Unorthodox Presentation of Scurvy Through Vasculitis and Pulmonary Hypertension

Background
Vasculitis, first described in 1866, describes a group of rare conditions that damage blood vessels leading to multiple organ dysfunction, affecting about 0.01% of the world’s population. Once experienced in practice, is a disease not forgotten. I will present a complicated case of C-ANCA/PR3 vasculitis.
Case Presentation
A 57-year-old female with a 40-pack year history of tobacco use, presented with complaint of fevers, malaise, and a painful purpuric rash, occurring after an earache one week prior. The rash started on her feet, later involving her torso and scalp. Four days after the rash started, she developed odynophagia with oropharynx ulcers.

Labs were consistent with acute kidney injury, anemia, elevated CRP, and sedimentation rate. She had proteinuria, hematuria and her infectious workup was negative. Initial skin biopsy showed a non-diagnostic vascular fluorescence pattern. By hospital day four, the C-ANCA/PR3 labs were positive. Initial chest CT showed diffuse tiny nodular infiltrate with larger irregular ground glass and nodular opacities and no pulmonary embolism. On day four, chest x-ray showed worsening severe diffuse bilateral alveolar lung disease, concerning for diffuse alveolar hemorrhage. 

She developed worsening dyspnea and escalating oxygen needs, requiring transfer to the critical care unit for respiratory failure. With positive C-ANCA/PR3 and her clinical presentation, she received pulse dose steroids with solumedrol 1,000mg for five days. She later had a cyclophosphamide infusion after developing an allergic reaction to rituximab. She required surgical debridement of her wounds and inpatient rehab, eventually being discharged home one month later with reduced but functioning kidneys. Although she was on DVT prophylaxis during hospitalization, she was readmitted two days afterwards with high-risk saddle pulmonary embolism requiring embolectomy.
Discussion
Our patient received pulse dose steroids four days after admission. With high clinical suspicion, it is appropriate to treat without biopsy results. Treatment with steroids, rituximab, and/or cyclophosphamide are common. She required surgical debridement of wounds, inpatient rehab and later an embolectomy. ANCA-associated vasculitis has a two-threefold increased risk of developing a thrombotic event. 

The gold standard for diagnosing vasculitis is kidney, lung, and/or skin biopsies. Due to her clinical picture and bleeding risk, we did not biopsy her kidneys or lungs. Her initial skin biopsy was non-specific, which is an inherent problem with skin sampling. Recognizing the history and physical exam of vasculitis is important for any specialty, allowing prompt laboratory testing, tissue biopsy, and coordination of the multiple specialties involved in the management of vasculitis.

When Earache’s Turn to Diffuse Alveolar Hemorrhage

Infantile Hyaline Fibromatosis Syndrome (also known as IHFS or Inherited Systemic Hyalinosis or ANTXR2-Related Hyaline Fibromatosis Syndrome) is a genetic condition characterized by deposition of hyaline in the skin, muscle, and viscera. IHFS is inherited in an autosomal recessive manner and characterized by mutations in the ANTXR2 (Anthrax Toxin Receptor 2) gene, resulting in the abnormal deposition of hyaline material in skin and organs. Symptoms can subsequently develop in multiple organ systems including rheumatological (progressive joint contractures), musculoskeletal (severe motor disability), immunological (increased susceptibility to infections), dermatological (thick, rough skin, hyperpigmented macules, nodules, and papules), and gastrointestinal (failure to thrive, nausea, vomiting, protein-losing enteropathy, failure to thrive). Complications from these can result in lifelong debilitation and early death.
Per FDA definition, it meets criterion for an ultra-rare condition, affecting fewer than 1 in 1,000,000 births throughout the United States and with fewer than 100 total cases reported worldwide. 

Here we present the case of a 4-month-old with a complicated medical history including painful extremity contractures, global developmental delay, neck hemangioma, and feeding intolerance who initially presented to our institution for abdominal distension. The multi-systemic, progressively worsening nature of her symptoms prompted consultation to inpatient pediatric genetics. Per their recommendation, rapid whole-genome sequencing (rWGS) was performed through Rady Children’s Hospital Institute for Genomic Medicine® in San Diego with the help of the Fabric GEM artificial intelligence (AI) tool. This revealed a homozygous pathogenic variant c.652T>C; P.Cys218Arg in the ANTXR2 gene consistent with IHFS.

This case was significant not only for its extreme rarity, but also its early manifestation of symptoms, wide range of affected body systems, and severity of symptoms, which together present a fascinating diagnostic dilemma for future clinicians that should be taken into consideration. It also highlights the increasing utility of AI-assisted rapid whole-exome sequencing as a diagnostic tool for medically complex patients with hitherto unknown multisystemic hereditary conditions.


An Ultra-Rare Disease: Infantile Hyaline Fibromatosis Identified Using AI-assisted Whole Genome Sequencing

Background

Diabetic kidney disease (DKD) is a complication of diabetes mellitus ultimately characterized by decreasing GFR and gradually increasing levels of proteinuria. In patients with T2DM and proteinuria studies have shown 53% of patients receive a pathologic diagnosis of non-diabetic renal disease when a biopsy is obtained. For this reason, it is important to consider kidney biopsy in diabetic patients with kidney injury and proteinuria whose presentation differs from typical DKD.

Case Presentation

A 77-year-old man with a past medical history including insulin-dependent type 2 diabetes mellitus, hypertension, and stage IV CKD presented with worsening left lower extremity weakness and pain. A history of diabetic retinopathy was notably absent. Additional testing showed an AKI with creatinine of 2.76 mg/dl (baseline of 2.11 mg/dl), hypoalbuminemia of 2.1 g/dl, protein of greater than 1000 mg/dl on urinalysis, and blood pressure of 192/104. A protein/creatinine ratio was elevated at 14.5, from 0.3 one year prior. A 24-hour urine protein was 11g, demonstrating nephrotic range proteinuria. A serologic workup for glomerulonephritis resulted normal C3 and C4, normal kappa/lambda ratio, negative ANA, ANCA, HBsAg, HBc IgM, HCV Ab, HIV, MPO and PR3 ANCA, PLA2R antibody and serum immunofixation demonstrating only hypoalbuminemia and hypogammaglobulinemia. HbA1c over the previous two years had been well controlled, between 5.3 and 6.8%. The patient’s creatinine remained stable at 2.8 mg/dl over the next week, and he was discharged on oral furosemide with plans for kidney biopsy. The presenting lower extremity symptoms were attributed to mild L5-S1 spinal stenosis and left tibial artery disease found on workup. Two weeks later the patient was readmitted with new onset shortness of breath, a 14kg weight gain and a creatinine of 3.99 mg/dl. Physical examination now showed 3+ bilateral lower extremity pitting edema and bibasilar crackles on lung auscultation. Aggressive diuresis was begun. Subsequent kidney biopsy showed C3 glomerulonephritis. The patient was discharged on an appropriate diuretic regimen with plans for outpatient management by nephrology.

Discussion

We present a case of rapidly progressive nephrotic range proteinuria in the setting of longstanding DKD which was secondary to biopsy proven C3 glomerulonephritis. This case underscores the importance of renal biopsy in patients with T2DM who develop renal disease in a pattern atypical of DKD, such as rapid onset nephrotic syndrome or severe kidney disease in the absence of diabetic retinopathy.


C3 Glomerulonephritis in a patient with nephrotic range proteinuria
and longstanding type 2 diabetes mellitus (T2DM)

Monoclonal gammopathy of renal significance encompasses renal disease in the nonlight chain disease manner in the presence of circulating monoclonal antibodies, likely without ongoing bone marrow proliferation. It has an acute course, variable presentation and needs to followed up on.

Monoclonal gammopathy of renal significance

Background

Amoxicillin-clavulanate can cause both liver injury and acute kidney injury. The
majority of the existing literature has described liver-related injury, with fewer
reports noting kidney injury. In this report, we describe a rare case of
concomitant drug-induced liver injury and acute interstitial nephritis as a result
of amoxicillin-clavulanate exposure.

Case Presentation

A 62-year-old male presented to the emergency department with weight loss,
nausea, and diarrhea. Two weeks prior to presentation, he was treated for
sinusitis with a ten-day course of amoxicillin-clavulanate (875 mg-125 mg)
twice daily. The patient was jaundiced, and his abdominal examination
revealed mild distension. Labs included a blood urea nitrogen of 98, creatinine
of 6.6 mg/dL, total bilirubin of 20.5, alkaline phosphatase of 397, aspartate
transaminase of 138, alanine transaminase of 88, and International Normalized
Ratio of 11.4 with pro-time of 127.9. A complete blood count was notable for
9.5% eosinophils, with a total level of 700 eosinophils. A computerized
tomography scan of the abdomen was performed, which revealed gallbladder
wall thickening; subsequent right upper quadrant ultrasonography showed a
minimally distended gallbladder and focally dilated intrahepatic ducts in the
left lobe of the liver. Given concern for renal failure, the patient was admitted
to the ICU. He was started on high-dose methylprednisolone for empiric
treatment of suspected autoimmune hepatitis. Given that drug-induced liver
injury was on the differential, tissue biopsies were obtained. A percutaneous
core kidney biopsy revealed acute tubular injury with bile cast nephropathy,
focal acute tubulointerstitial nephritis, moderate arteriolar hyalinosis, and mild
arteriosclerosis. The liver biopsy showed bile pigment within hepatocytes and
bile canaliculi in peri-central vein areas. These biopsy findings were suggestive
of amoxicillin-induced renal and hepatic injury. The patient was continued on
high-dose IV steroids (which he received for a total of five days) that were
transitioned to an eighteen-day oral prednisone taper. His creatinine gradually
normalized, and the patient’s LFTs remained mildly elevated on the day of
discharge.

Discussion 

This case study demonstrates a rare occurrence in which a patient developed drug-induced liver injury and renal failure. Though antibiotics are widely used to treat infection, their use is not without consequences. In our case, the pathology revealed findings consistent with the immuno-allergic response in amoxicillin-clavulanate drug-induced injury. As this relays the etiology behind the multiorgan failure, tissue biopsy is an essential component in guiding the treatment of patients afflicted with concomitant hepatic failure and renal failure caused by amoxicillin-clavulanate.

Utility of Tissue Biopsy in Amoxicillin-Clavulanate Induced Hepatic Failure and Renal Failure

Single-energy computed tomography (SECT) head is a common diagnostic tool to evaluate for intracranial hemorrhage in emergency settings due to its widespread accessibility and non-invasive nature. However, SECT has densitometric evaluation limitations. For example, hyperdensities on SECT such as blood product and iodine contrast appear similarly. Dual-energy CT (DECT) is a relatively under-utilized imaging modality that has the capability to differentiate between multiple materials. This imaging technique can be extremely useful in identifying materials that are otherwise indistinguishable from standard SECT.

The authors present a case of a patient with findings suspicious of intraventricular and subarachnoid hemorrhage on conventional SECT. The suspected hemorrhage was subsequently ruled out utilizing DECT, as iodinated contrast can be subtracted out, yielding an image that can differentiate iodine contrast from blood or other hyperdense material. The authors discuss the underlying physics, potential advantages, and limitations of the DECT.


Utility of Dual Energy CT Head to Differentiate Myelography Contrast from Intraventricular and Subarachnoid Hemorrhage

Background
Guillain-Barré Syndrome (GBS) is a rare autoimmune disorder of the peripheral nervous system, classically characterized by symmetric, ascending muscle weakness that can progress to life-threatening respiratory depression. Diminished sensation, paresthesia, and autonomic dysfunction may also occur. GBS is a dysregulated immune response triggered by infections.  

Case Presentation
A 15-year-old male with history of depression and substance use presented to the emergency room with one week of bilateral leg weakness, dyspnea, and migratory joint pains. One month prior, he had an upper respiratory infection which resolved spontaneously. Patient was travelling when he developed gait instability, dysarthria, photophobia, and shortness of breath. CT Head was normal. His respiratory function worsened, requiring escalating oxygen requirements, followed by acute deterioration of mental status. He was sedated, put on ventilatory support, and transferred to our critical care unit.  

Neurological exam revealed hypotonia, present reflexes, and poor muscle coordination out of proportion to muscle weakness, which initially suggested functional etiology. MRI and MRA brain and spine were unremarkable. Cerebral spinal fluid studies revealed albuminocytologic dissociation and elevated inflammatory markers (IL-6, IL-8). Potential autoimmune, paraneoplastic, rheumatologic, demyelinating, infectious, and toxic causes were ruled out. After unsuccessful extubation attempts, serial examination revealed involvement of cranial nerves VII, IX, and X. 

He received a three-day course of intravenous immunoglobulin (2g daily) and gabapentin. Major complications included hospital acquired pneumonia and decompensated psychiatric state (worsening mood, panic attacks). Over three weeks, his mental status normalized, and he regained significant muscle strength and coordination. After confirming regained diaphragmatic function on ultrasound, he was extubated and weaned to room air. The patient was then transferred in stable condition to an acute rehabilitation center. 

Discussion
In pediatric patients, clinicians should conceptualize GBS as a spectrum of neurological symptoms that can differ from the typical ascending pattern but remain responsive to immunoglobulin treatment. This case proved unique because our patient’s history aligned with classic GBS, but he did not have expected radiological findings and patchy, rather than length-dependent, motor and sensory symptoms. His presentation had mixed features of multiple GBS subtypes, including Acute Motor Axonal Neuropathy and Multifocal Acquired Demyelinating Sensory and Motor Neuropathy. In addition to diaphragmatic weakness, patients can develop cranial neuropathies that prolong need for mechanical ventilation and increase risk of pneumonia. Lastly, in adolescents with prior psychiatric history, GBS can acutely exacerbate mood and anxiety symptoms which may be falsely attributed to functional neurological disorder.

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