This is a case of two rare entities causing non-specific symptoms. Carotid-cavernous sinus fistula (CCF) arises from miscommunication of carotid arterial flow and the cavernous sinus. Post traumatic CCF presents bilaterally are uncommon, only 1-2% of patients. While already a rare diagnosis, our patient presented in an acute parathyroid crisis defined by symptomatology caused by markedly elevated calcium and parathyroid hormone, which may have masked our diagnosis of CCF.CASE PRESENTATION: A 57-year-old Colombian female presented with dizziness, anorexia, nausea, and vomiting. She also endorsed intermittent diplopia in the left eye. Physical exam revealed left sided ptosis. She reports a remote history of head trauma a month prior. Serum calcium on presentation was 13.6 mg/dL, ionized calcium of 6.8 mg/dL, and parathyroid hormone (PTH) was 219.8 pg/mL. Subsequently, a Technetium 99m sestamibi scan showed increased radioisotope along the right lower pole of the thyroid gland confirming primary hyperparathyroidism. She was resuscitated with normal saline fluid and started on Cinacalcet for hypercalcemia. Attempts to lower serum calcium can be achieved using bisphosphonates and may be effective within the first 24 hours. In our patient, Cinacalcet did not achieve sufficient calcium lowering thus, Zoledronic acid was used due to its potency with small doses. Nausea, vomiting, and positional dizziness resolved. Despite resolution of symptoms, she continued with ptosis; thus prompting further work up. Magnetic resonance angiography and venography revealed extensive time of flight enhancement throughout the bilateral cavernous sinuses. A cervical and cerebral angiography revealed bilateral carotid cavernous fistulas with ophthalmic vein arterialization. The next day, she underwent left cavernous sinus embolization with coiling. Parathyroidectomy was delayed due to recurrence of ptosis and need for a second embolization for persistent diplopia that resulted in resolution of symptoms.DISCUSSION: Each of these diagnoses are rare and both require timely evaluation and treatment. The patient's symptoms are classically seen in a parathyroid crisis, with nausea, vomiting, and anorexia being the most common symptoms in up to 48% of parathyroid crises. Like the aforementioned, CCF symptomatology also includes non-specific symptoms; however, may pose more of a challenge during diagnosis as symptoms wax and wane depending on the hemodynamic flow within the fistula.CONCLUSIONS: This case highlights the necessity of a thorough physical exam and further as a reminder that a clinician must be vigilant in ruling out alternative pathologies supported by the objective findings no matter how rare or unlikely.
Hydroxyzine primarily treats pruritus, anxiety, and insomnia due to its ability to bind histaminic, muscarinic, serotonergic, and dopaminergic receptors. Here, we present a case of rare manifestations of hydroxyzine overdose.CASE PRESENTATION: A 30-year-old female presented after a suicidal attempt with presumptive amlodipine overdose. She was found tachycardic, tachypnic, hypotensive, and lethargic. Urine and serum drug screen was negative. Blood gas revealed a non-anion gap metabolic acidosis. Chest x-ray (CXR) showed no anomalies. ECG revealed sinus tachycardia with normal QT interval. A head CT showed no anomalies. Crystalloid fluid resuscitation was initiated for presumptive amlodipine overdose induced hypotension. Norepinephrine (NE) drip was initiated for distributive shock. Day 1, she complained of excessive thirst and urinary retention; CXR showed bilateral diffuse infiltrates. Echocardiogram revealed left ventricular ejection fraction of 60-65% without wall motion abnormalities or valvulopathy. Day 2, she developed delirium and visual hallucination, warm and dry, intermittent hypotension, large A-a gradient, PaO2/FiO2 ratio <100, and worsening bilateral infiltrates on CXR; consistent with severe ARDS requiring intubation. Clinical presentation was suspicious for anticholinergic toxicity. External records revealed a 120-tablet hydroxyzine 25 mg prescription, and the family provided an update revealing an empty bottle of 90 tabs of hydroxyzine 25mg at home. There was no role for hemodialysis or hemoperfusion. She required maximal support on NE, vasopressin, phenylephrine, and dopamine for worsening distributive shock. Due to persistent anticholinergic symptomatology, two trials of physostigmine were administered with transient avail. Day 3, she required maximal ventilator support for worsening hypoxemia and was referred for ECMO. Day 4, she was slowly weaned off of dopamine, phenylephrine and NE prior to transfer to the ECMO facility. After transfer, she was weaned off of vasopressin, extubated, and discharged home prior to the initiation of ECMO.DISCUSSION: In young adults, hydroxyzine has a 20-hour half life. Our patient ingested about 2 grams of hydroxyzine. The diagnosis of anticholinergic toxicity may be confirmed by resolution or improvement of symptoms during a slow IV injection of 0.5 to 1 mg of physostigmine salicylate. General supportive care and seizure control with physostigmine and diazepam may result in complete recovery within 72 hours.CONCLUSIONS: Hydroxyzine is a safe and effective drug, but life-threatening adverse effects can occur with overdose. Symptoms of toxicity are delirium, seizures, tachycardia, and hypotension. High dose of hydroxyzine may cause ARDS and distributive shock. A postmortem analysis of a confirmed hydroxyzine overdose demonstrated severe pulmonary edema, hyperemia and occasional alveolar hemorrhage.
INTRODUCTION: Mycoplasma pneumoniae (MP) is a common cause of community acquired pneumonia with an incidence of 1-3 per 1000 cases annually [1]. However, extrapulmonary manifestations of MP in the adult population are rare [3]. The mechanism behind injury is predicted to be caused by bacterial inflammation and vascular occlusion combined with an autoinflammatory response [2]. We present a case of a 21-year-old Hispanic male with rhabdomyolysis and peri-myocarditis caused by MP. CASE PRESENTATION:A 21-year-old Hispanic male with a past medical history of Kawasaki disease presented complaining of constant chest pain for two days. He endorsed subjective fever, dark urine, and myalgias. He had previously visited an urgent care and was prescribed ibuprofen and cyclobenzaprine to no avail. On physical exam, the patient was afebrile and tachypneic. Cardiac exam revealed tachycardia with no rubs, murmurs, or gallops. Lung fields were clear to auscultation bilaterally. Chest pain was not reproducible upon palpation. The abdomen was soft, nondistended, and without organomegaly. Initial labs revealed leukocytosis, transaminitis, elevated d-dimer, elevated troponins, elevated C-reactive protein, and elevated creatinine kinase. Admission chest x-ray was without infiltrates, cardiomegaly, or pneumothorax. Initial electrocardiogram demonstrated ST elevations in inferolateral leads. Emergent cardiac catheterization demonstrated normal coronary anatomy. CTA of the chest was negative for pulmonary embolism and aortic dissection. Original echocardiogram demonstrated normal ejection fraction. Respiratory pathogen panel was positive for MP IgM. Treatment for MP-induced rhabdomyolysis and peri-myocarditis with intravenous fluids and azithromycin was initiated. He experienced a transient systolic heart failure, managed with Bilevel Positive Airway Pressure. The rapid clearance of bacteria with proper antibiotics allowed the stunned myocardium to recuperate within 72 hours. At which point the patient experienced rapid clinical improvement and was discharged home in stable condition. DISCUSSION:The diagnosis of MP is difficult due to its cellular structure, its ability to be missed on routine blood cultures, and its ability to cause extrapulmonary manifestation via autoimmune dysfunction [2]. The case demonstrates a patient with rhabdomyolysis and peri-myocarditis with positive MP IgM. The patient also experienced rapid clinical improvement with clearance of bacteria by antibiotic administration. Thus, we were able to diagnose another rare manifestation of a MP infection causing rhabdomyolysis and peri-myocarditis.CONCLUSIONS: MP is difficult to isolate and has the ability to present with myriad symptomatology. Although MP is difficult to diagnose, it is easily treated. Therefore, MP should be considered in young patients due to its increased incidence in the younger population and unique presentations.
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