Patient: Male, 44-year-old Final Diagnosis: COVID-19 • Guillain-Barré syndrome Symptoms: Facial paralysis Medication: — Clinical Procedure: — Specialty: Critical Care Medicine • Medicine, General and Internal • Neurology Objective: Rare disease Background: This case report is of a patient who presented with loss of taste and facial weakness and was diagnosed with Guillain-Barré syndrome (GBS) and Bell’s palsy, associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. GBS is a neurological emergency defined as acute inflammatory demyelinating polyneuropathy. The patient responded to intravenous immunoglobulin (IVIG) treatment. Case Report: We present the case of a 44-year-old Hispanic man who came for evaluation of bilateral facial weakness and lack of taste sensation. He had lower motor neuron facial weakness. His head computed tomography and brain magnetic resonance imaging scans did not show any pathological abnormalities. He tested positive for SARSCoV-2 by a nasopharyngeal swab reverse transcription polymerase chain reaction (RT-PCR) test. Cerebrospinal fluid (CSF) analysis via lumbar puncture revealed elevated protein levels, no leukocytes, and a negative Gram stain. The CSF RT-PCR test for SARS-CoV-2 was negative. PCR tests of the CSF for other viral infections were negative. A diagnosis of GBS was made, and he was treated successfully with IVIG. After the fourth dose of IVIG, the patient was able to close his eyes, frown, show his teeth, and smile. Conclusions: Our case is rare because the patient did not present with lower extremity weakness, but only with bilateral Bell’s palsy. Physicians should be aware of GBS because it is a neurological emergency for which COVID-19 can be a risk factor. Early diagnosis and treatment of GBS can prevent neurological disability.
Patient: Male, 50Final Diagnosis: Acute colonic pseudo-obstructionSymptoms: Abdominal pain • cough • feverMedication: —Clinical Procedure: Colonoscopy decompression and colectomySpecialty: Critical Care MedicineObjective:Rare co-existance of disease or pathologyBackground:Acute colonic pseudo-obstruction (ACPO) is an infrequent entity characterized by non-toxic, non-mechanical, abrupt, functional dilation of the colon. Clinically patients present with abdominal distention, anxiety, severe abdominal pain, nausea, and vomiting. This rare entity can lead to a fatal outcome if not recognized early. A high level of suspicions is paramount for early diagnosis and prompt intervention.Case Report:A 50-year-old male was admitted to the intensive unit care due to acute hypoxic respiratory failure, pneumonia, and septic shock requiring mechanical ventilation and intravenous vasopressors. Two weeks after admission, his clinical course deteriorated and was complicated with acute abdominal distension, pain, and ileus. Imaging confirmed acute onset of ileus and after ruling out metabolic and infectious causes, the diagnosis of ACPO was made. Aggressive medical and surgical management resulted in a favorable outcome.Conclusions:Critically ill patients on ventilator are commonly sedated; therefore, usual symptoms of ACPO can be missed or misinterpreted leading to late diagnosis with increased morbidity and mortality. Clinicians must be aware of potential harm and side effects from common sedatives used in the intensive care unit and should be current on medical literature. Alpha-2 agonists, i.e., dexmedetomidine, is increasingly been used in critical care setting and there are few reports of a possible association with ACPO. We present here a case of a patient with dexmedetomidine-induced ACPO, and we provide a review of the existing literature and pathophysiology of the condition.
Background Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome are two forms of thrombotic microangiopathies. They are characterized by severe thrombocytopenia, microangiopathic hemolysis, and thrombosis, leading to a systemic inflammatory response and organ failure. Plasmapheresis is used to treat thrombotic microangiopathies. A different entity known as atypical hemolytic uremic syndrome has garnered more clinical recognition because reported cases have described that it does not respond to standard plasmapheresis. Diclofenac potassium is a non-steroidal anti-inflammatory drug that is used to treat pain. Case report A 35-year-old Hispanic man presented to our emergency department with complaints of generalized malaise, fever, and an evanescent skin rash. During admission, he reported the use of diclofenac potassium for back pain on a daily basis for 1 week. He was noted to have peripheral eosinophilia, so he was admitted for suspected drug reaction involving eosinophilia and systemic symptoms. His initial laboratory work-up showed microangiopathic hemolytic anemia and thrombocytopenia. He also experienced a seizure, encephalopathy, and had a PLASMIC score of 7, thus raising concerns for thrombotic thrombocytopenic purpura. He underwent emergent plasmapheresis, which improved his clinical condition. The diagnosis was confirmed by assessing the levels of disintegrin and metalloproteinase with thrombospondin type 1 motif, member 13, which was less than 3%. In addition, his skin biopsy was positive for patchy complement deposition, demonstrating complement dysregulation. Conclusion Thrombotic thrombocytopenic purpura is a rare condition that can be acquired. Our case is rare because it represents the first report of diclofenac potassium-induced thrombotic thrombocytopenic purpura with subjacent complement activation and dysregulation. Early recognition and aggressive management led to a favorable outcome.
A localized left atrial tamponade caused by left side pleural effusion is a rare finding that leads to hemodynamic instability. Here, we describe left atrial systolic and diastolic collapse resulting from left pleural effusion. An increase in intrapleural pressure by a pleural effusion can compress the pericardial space and lead to impaired cardiac filling and tamponade physiology. Here, we present a case of a 79-year old African American female who presented with shortness of breath and dry cough for a duration of one week. Chest radiograph and CT scan of the chest showed left pleural effusion. The echocardiogram revealed left atrial systolic and diastolic collapse due to pleural effusion, which triggered cardiac tamponade physiology. With the guidance of a bedside thoracic ultrasound, she underwent a diagnostic and therapeutic thoracentesis which resolved her symptoms. Repeat echocardiogram revealed resolution of the cardiac tamponade with no further indication of left atrial diastolic collapse. In conclusion, pleural effusions can cause tamponade physiology and can be resolved by thoracentesis. Early recognition by a bedside point-ofcare ultrasound may help provide prompt relief of tamponade.
Introduction Pasteurella multocida is a gram-negative coccobacillus pathogenic to animals. It can cause infection in humans by a bite, scratch, or lick from a cat or dog. P. multocida can cause a variety of infections in humans, including cellulitis, osteomyelitis, endocarditis, peritonitis, and septic shock. Case Presentation A 56-year-old male presented to our hospital with a 2-day history of fever, abdominal pain, nausea, and vomiting. He denied exposure to cats, dogs or other pets. He had severe respiratory distress requiring ventilator support, profound septic shock requiring multiple vasopressors, severe lactic acidosis, and renal failure requiring emergent hemodialysis. Blood cultures confirmed the presence of P. multocida. The patient subsequently died of cardiopulmonary arrest due to multiorgan failure with refractory shock. Conclusion P. multocida septicemia can lead to septic shock. Early identification of this organism may decrease mortality. Although our patient had no known cat or dog exposure, physicians should enquire about a history of animal exposure when a patient presents with an infection with no obvious cause.
Background The efficacy and safety of etanercept (ETN) has been demonstrated in patients with juvenile idiopathic arthritis (JIA) from 4 years, although more data are needed regarding the population under 4 years old. Objectives The aim is to evaluate the efficacy and safety of etanercept in patients under 4 years old diagnosed with polyarticular JIA and to assess the adherence to drug treatment in this population. Methods We analyzed retrospectively, from medical records of patients, the following variables: epidemiologic data, number of active and limited joints at baseline and at 6 months; we also registered laboratory parameters including CRP, ESR, iron and hemoglobin. Other variables recorded were CHAQ punctuation; physician and parents global assessment at baseline and 6 months of treatment. Continuous variables are presented as means±SD. Results From a total of 25 patients with JIA younger than 4 years old treated with ETN only 21 were analyzed. There were 14 girls and 7 boys with a mean age at diagnosis of 23±19.4 months. All patients had received methotrexate (MTX), corticosteroids (prednisolone) and ETN (0.8mg/kg/wk) as initial therapy. The mean duration of treatment with etanercept was 36.6±22 months.Iron laboratory values at baseline were low (49.89±25.6μg/dl) but normalized at 6 months of treatment (70.76±31.2μg/dl). Number of active and limited joints at baseline were 12±4.3/3.5±5.1 respectively; at six months of treatment were 1.44±1.77/1±1.33.CHAQ punctuation at baseline was 1.2±0.3 and 0.4±0.2 at six months. Physician and parents’global assessment at baseline were 71.5±11.5/70±14.1 respectively and 11.6±11.2/12.9±12.4 at 6 months of treatment. CRP and ESR parameters at baseline were 40.8±24.1 mg/l/51.9±19.4 mm/h respectively and 3±4.9 mg/l/14.1±8.3mm/h at six months of treatment. All patients achieved clinical remission at 6 months of treatment. Furthermore, in all patients discontinuation of therapy with corticosteroids was performed and 60% achieved discontinuation of MTX after 6 months of treatment. ETN was discontinued in 2 patients (9.5%) due to remission of the disease: one outbreak must be restarted on therapy after 3 months and the other remains in remission without treatment a year later. Four patients (19%) remained at doses below 0.8mg/kg/wk. Any patient had serious adverse effects secondary to treatment. Conclusions Although important joint involvement and alteration of analytical parameters at baseline a high percentage of patients achieved remission at 6 months of treatment with etanercept. All patients could reduce concomitant medication and dose reduction or withdrawal of etanercept was possible in some patients. Treatment with etanerceptin patients under 4 years old is shown as safe and effective in our patient group after 6 months of treatment. Disclosure of Interest None Declared
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