49 yo Augusta gentleman seeks woman 25 45

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Try out PMC Labs and tell us what you think. Learn More. Hester 1 ; V. Martin 1 ; S. Bansil 1 ; C. Fichtenbaum 1. Tracking ID Recognize the clinical setting of acyclovir-induced neurotoxicity. Diagnose and manage acyclovir-induced neuroxicity. Doppler ultrasounds were negative for deep venous thrombosis on two different tests. She had been in stable health without recent opportunistic infections. Her past medical history was ificant for a history of shingles, orolabial herpes simplex disease, pancreatitis secondary to nucleosides, Candida esophagitis, and asthma.

A small vesicle has preceded the ulcer. Laboratory data included a white blood cell count of 8. The Alveolar-arterial gradient was Computerized Tomography of the right lower extremity with contrast and multiplanar 3D reconstructions revealed no abscess. The next day the patient developed delirium and hypoxemia. The arterial blood gas revealed a pH 7.

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Chest radiography demonstrated pulmonary edema. Cultures of the peritoneal fluid, bronchoalveolar lavage, blood, and spinal fluid, were all negative. The skin biopsy demonstrated findings consistent with calciphylaxis and pressure necrosis and the absence of viral inclusions. Acyclovir was discontinued on the sixth hospital day and a serum acyclovir level 12 hours after stopping the acyclovir was 5.

Twenty-four hours after stopping the acyclovir the patient became alert and was extubated within 48 hours. Given all of these findings, the patient was diagnosed with acyclovir-induced respiratory depression. Neurotoxicities such as lethargy, confusion, and delirium have been reported with acyclovir and seem to be more prevalent in the setting of kidney dysfunction, but have been identified in otherwise healthy individuals. To our knowledge, this is the first case report of acyclovir leading to respiratory failure in a patient with chronic renal disease. As demonstrated in this case, acyclovir should be used cautiously in those with renal failure to prevent neurotoxicities.

Adams 1. Review Amiodarone's effects on thyroid function. Diagnose and treat thyrotoxic effects of Amiodarone. The patient was started on Amiodarone 2 years ago for paroxysmal atrial fibrillation and had remained in sinus rhythm without further complications. Upon initial work-up patient was found to have an undetectable TSH, and an elevated free T4.

Hypothyroidism occurs by several mechanisms, the most common being a destructive thyroiditis which is often preceded by a hyperthyroid phase. Additionally, Amiodarone decreases the peripheral conversion of T4 to T3 and acts to directly block the T3 receptor. Lastly, synthesis of thyroid hormone is inhibited by high levels of iodine in Amiodarone Wolff-Chaikoff effect.

Treatment of hypothyroidism is with replacement therapy and is rarely an indication to discontinue therapy. Hyperthyroidism secondary to Amiodarone toxicity also occurs by a variety of mechanisms. In Type 1, synthesis of T4 is increased due to iodine load in a patient with underlying autonomy secondary to a nodule or goiter. In Type 2, patients develop a destructive thyroiditis often followed by hypothyroidism. Clinically, determining the mechanism of hyperthyroidism can be challenging but can direct therapy. Detectable uptake on thyroid scan or nodules on exam suggest Type 1.

Patients with Type 2 sometimes have elevated IL-6 levels. Type 1 disease is treated with anti-thyroid drugs such as Methimazole and response may be slow. 49 yo Augusta gentleman seeks woman 25 45 with Type 2 are treated with steroids and often respond quickly. In clinical practice, patients are often treated with both, with the rapidity of response guiding further treatment. In considering stopping therapy, it is important to weigh the risks of chronic hyperthyroidism against the risk of arrhythmia.

Amiodarone has a very long half-life which prevents any immediate benefit in stopping the drug, and symptoms may actually be exacerbated when the beta-blocking effects of Amiodarone are lost. In general, thyrotoxicity is not an absolute contraindication for continuation of Amiodarone and risks and benefits must be weighed carefully. Younes 1 ; R. Parker 1. He reported the problem starting while he was on a plane trip from Denver to Pittsburgh where he felt some shortness of breath with mild headache. When he reached Pittsburgh, he couldn't tell where he came from, or the time of the day.

He was even somewhat confused about his personal belongings. This episode was followed with several incidences of forgetfulness in his daily tasks, such as forgetting the water tap was open and forgetting his daily schedule of activities. Physical exam revealed no localized neurological deficit. An MRI of brain showed no evidence of a new ischemic or hemorrhagic stroke, although it showed an old right MCA occipital lobe infarct.

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A hypercoagulable workup was negative. WBC count was 6.

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A repeat CBC confirmed above values. Serum viscosity and erythropoitin level proved normal. A blood volume study showed normal RBC volume, with a low plasma volume, and a low normal total blood volume; all findings consistent with a relative polycythemia. In view of the persistent neurological findings, therapeutic phlebotomy of the patient was done, with ml removed each time.

After a few sessions, the patient reported his symptoms improving ificantly, with a decrease in his hemoglobin and hematocrit levels. Possible causes of this relative polycythemia include dehydration, alcohol, smoking, obesity, hypoxia, acute MI, and hypertension. PV is known to cause both microvascular disturbances, such as peripheral ischemia and atypical cerebral ischemic attacks, as well as major arterial and venous thromboembolism.

However, the risk of vascular occlusive episodes in relative polycythemia is not well known. A study by Schwartz et al. The fact that our patient's symptoms improved after phlebotomy as his hematocrit decreased, suggests that his symptoms were atypical cerebral attacks.

Although phlebotomy is not considered a typical treatment modality of relative polycythemia, it worked well with our patient. Divakaruni 1 ; A. Hwang 2. Recognize Camplyobacter species as a potential etiology of bacterial meningitis in patients with predisposing illness, including recent or distant neurosurgery, or alcohol abuse.

Treat CNS infections with C. Campylobacter is an uncommon cause of bacterial meningitis in adults. We report the case of a year old Vietnamese gentleman with a prior history of partial craniotomy and alcohol abuse who was admitted with headache, fever, neck pain, and weight loss over the preceding two weeks. The patient had reported a history of a flu-like illness preceded by one day of non-bloody diarrhea, but these symptoms had resolved several days prior to admission. On admission, he was febrile to The fluid was India ink negative, cryptococcal antigen negative, and acid-fast bacilli negative.

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The patient was initially treated with intravenous vancomycin and cetriaxione. On the third hospital day, one out of four blood cultures began to grow out gram-negative rods. The subsequent day, the patient's cerebrospinal fluid grew out comma-shaped gram-negative rods suspicious for Campylobacter species.

Vancomycin was discontinued, and the patient was started on gentamicin in addition to ceftriaxone. The patient responded rapidly to antibiotic therapy. Both the patient's blood and cerebrospinal fluid cultures eventually returned with a final result of Campylobacter fetus species. The patient was treated with a total of five days of parenteral gentamicin, fifteen days of parenteral ceftriaxone, and an additional seven days of oral ciprofloxacin for a total antibiotic course of twenty-one days. At the time of discharge the patient was doing well, and had no further gastointestinal or neurologic symptoms.

In this case of Campylobacter fetus meningitis, the patient had predominately extra-intestinal manifestations as is normally seen with C. The patient had a predisposing immunosuppressed state secondary to his alcohol abuse, as well as a prior history of neurosurgery, consistent with ly reported cases. Given the incidence of mortality reported in the case literature, and this patient's rapid response to the selected antibiotic regimen, the early and appropriate treatment of C. Ramamurthy 1 ; M. Graham 2. Viral pathogens can cause a variety of syndromes when affecting the central nervous system including aseptic meningitis and encephalitis.

Varicella zoster virus VZV is a rare cause of central nervous system syndromes.

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We discuss a patient who initially presented with dermatomal zoster whose clinical course was complicated by the development of VZV encephalitis with complications both from the primary disease process and the appropriate therapy. Seven days prior to admission she developed an erythematous rash on back and chest confined to right side of thorax. She was treated with valacyclovir for two days and complained of pain at the site for which she was prescribed vicodin and amitryptyline. The next day she was noted to be disoriented by family and brought to ER.

Physical exam revealed an erythematous vesicular rash on her chest and back confined to the T2—T3 dermatome on right side. Neurological exam was within normal limits except that she had difficulty finding words. On day 3 her creatinine level increased and urinalysis revealed numerous crystals consistent with acyclovir induced nephropathy.

The acyclovir dose was adjusted based on renal function and she was given IV fluids. On day 4 she complained of hallucinations and double vision. MRI of the head was normal. She continued to improve with IV acyclovir and hyponatremia resolved. Patient completed a two week course of IV acyclovir and was discharged on oral valacyclovir for an additional week and neurontin for pain. Herpes zoster encephalitis is rare and very few cases have been reported. We postulate that in this case her immunosuppresed state on methotrexate was the main predisposing factor.

This case also highlights the complications of disease process, specifically hyponatremia SIADH and adverse effect of treatment acyclovir induced nephropathy and how to manage them astutely.

49 yo Augusta gentleman seeks woman 25 45

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