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Abstract

A case is described of a 29-year-old female who presented with acute hypoxic respiratory failure due to acute eosinophilic pneumonia, associated with the use of electronic cigarettes to vape tetrahydrocannabinol (THC), together with the contemporary clinical understanding of the syndrome of electronic-cigarette associated lung injury (EVALI). Attention is drawn to acute eosinophilic pneumonia as a potential consequence of vaping-associated lung injury to understand the diagnostic evaluations and therapeutic interventions for acute eosinophilic pneumonia associated with vaping THC.

Abstract

The novel coronavirus disease, 2019 (COVID – 19) evolved as an unprecedented pandemic. The severe acute respiratory syndrome-corona virus-2 (SARS-CoV-2) infection has been associated with significantly deranged coagulation parameters and increased incidence of thrombotic events. Deranged coagulation parameters, such as D-dimers and fibrin degradation products, can indicate a poor prognosis, and their measurement will help stratify the patients according to the disease severity, need of intensive care unit admission, and prediction of the clinical course. Gaps in understanding the natural history of the disease cause difficulties in tailoring therapies and optimizing the management of patients. Lack of specific treatment further complicates this situation. While thrombotic events can cause significant morbidity and mortality in patients, a focused approach to the prevention and treatment of venous thromboembolism (VTE) can, to a great extent, decrease the disease burden caused by thrombotic diseases. Pharmacological prophylactic anticoagulants and mechanical therapies such as pneumatic compression devices can help prevent venous thromboembolism and other thrombotic events. Thrombotic events due to COVID-19, their prevention and management, are the focus of this paper, with the prospect of providing insights into this relatively unexplored area.

Abstract

Objective

A rare variant Miller Fisher Syndrome overlap with Guillain Barre Syndrome is described in an adult patient with SARS-COV-2 infection.

Case Presentation

The clinical course of a 45-year-old immunosuppressed man is summarized as a patient who developed ataxia, ophthalmoplegia, and areflexia after upper respiratory infection symptoms began. A nasopharyngeal swab was positive for COVID-19 polymerase chain reaction. He progressed to acute hypoxemic and hypercapnic respiratory failure requiring intubation and rapidly developed tetraparesis. Magnetic resonance imaging of the spine was consistent with Guillain Barre Syndrome. However, the clinical symptoms, along with positive anti-GQ1B antibodies, were consistent with Miller Fisher Syndrome and Guillain Barre Syndrome overlap. The patient required tracheostomy and had limited improvement in his significant neurological symptoms after several months.

Conclusions

The case demonstrates the severe neurological implications, prolonged recovery and implications in the concomitant respiratory failure of COVID-19 patients with neurological symptoms on the spectrum of disorders of Guillain Barre Syndrome.

Abstract

Introduction

In acute myeloblastic leukaemia (AML) explosive proliferation and accumulation of immature myeloid cell clones take place, replacing the bone marrow, with the possibility of the formation of extramedullary tumour masses composed of myeloid cells. The onset of the disease less frequently consists of symptoms of extramedullary manifestation.

Case presentation

A Caucasian male child aged three years and 11 months was hospitalized for bilateral exophthalmos and otorrhea, due to an alteration in his general condition. Ocular ultrasound revealed an inhomogeneous thickening of the upper right muscles superior to the eyeball. A complete blood count showed severe anaemia, leucocytosis with neutropenia and thrombocytopenia. A peripheral blood smear evidenced myeloblasts. The result of the cytology of bone marrow confirmed the diagnosis of AML. Following blood product replacements and cytostatic treatment (AML-BFM 2004 HR protocol), the remission of exophthalmos and the correction of haematological parameters were favourable.

Conclusion

In a child with a sudden onset of exophthalmia and altered general condition, the diagnosis of acute leukaemia should be considered. The importance of performing a peripheral blood smear and bone marrow examination is emphasized so that diagnosis and initiation of treatment are not delayed.

Abstract

Introduction

Quetiapine is commonly used in intensive care units (ICU) to treat delirium. Cardiopulmonary arrest caused by low dose quetiapine is unreported. Only two cases in the literature have reported acute respiratory failure after single doses of 50mg and 100mg respectively. We report a case of cardiopulmonary arrest in a patient after the administration of a single 25mg dose of quetiapine.

Case presentation

A 72-year-old Chinese female with multiple cardiovascular co-morbidities was admitted to the ICU intubated, following complications from an elective endovascular repair of an infrarenal abdominal aortic aneurysm. She was alert and extubated the following day. She subsequently showed signs of delirium and was administered a single 25mg dose of oral quetiapine. Seven hours after ingestion, she developed type 2 respiratory failure and eventually cardiopulmonary arrest. She was successfully resuscitated and other causes for cardiopulmonary arrest were excluded. Twenty-four hours following her cardiopulmonary arrest, her respiratory failure had completely reversed and she was extubated uneventfully.

Conclusion

This case report demonstrates that a single dose of oral quetiapine 25mg is sufficient to cause respiratory failure and cardiopulmonary arrest. Caution is advised when prescribing quetiapine in the elderly, especially in those with impaired drug clearance.

Abstract

Background

Vasopressors are conventionally administered through a central venous catheter (CVC) and not through a peripheral venous catheter (PVC) since the latter is believed to be associated with increased risk of extravasation. Placement of a CVC requires suitably trained personnel to be on hand, and in resource-limited settings, this requirement may delay placement. Because of this and in cases where suitably trained personnel are not immediately available, some clinicians may be prompted to utilise a PVC for infusing vasopressors. The objective of this study is to assess the feasibility and safety of vasopressors administered through a PVC.

Materials and methods

Patients who received vasopressors through a PVC for more than one hour were included in a single centre, consecutive patient observational study. Patients with a CVC at the time of initiation of vasopressors were excluded. Data regarding the size, location of PVCs, dose, duration and number of vasopressors infused were recorded. The decision to place CVC was left to the discretion of the treating physician. Extravasation incidents, severity and management of such events were recorded.

Results

One hundred twenty-two patients age 55(4) years [mean (SD)] were included in the study. The commonest PVC was of 18G calibre (57%), and the most common site of placement was the external jugular vein (36.5%). Noradrenaline was the most common vasopressor used at a dose of 10.6 (7) mcg/min [mean (SD)] and the median duration of nine hours (IQR: 6-14). CVC was placed most commonly due to an increasing dose of vasopressors after 4.5(4) hours [mean (SD)]. Grade 2 Extravasation injury occurred in one patient after prolonged infusion of fifty-two hours, through a small calibre (20G) PVC, which was managed conservatively without any sequelae.

Conclusion

Vasopressors infused through a PVC of 18G or larger calibre into the external jugular, or a forearm vein is feasible and safe. Clinicians need to balance the safety of peripheral vasopressor infusion with the additional costs and complications associated with CVC in resource-limited settings.

Abstract

COVID-19 has resulted in unprecedented global health and economic challenges. The reported mortality in patients with COVID-19 requiring mechanical ventilation is high. VV ECMO may serve as a lifesaving rescue therapy for a minority of patients with COVID-19; however, its impact on overall survival of these patients is unknown. To date, few reports describe successful discharge from ECMO in COVID-19 after a prolonged ECMO run. The only Australian case of a COVID-19 patient, supported by prolonged VV ECMO in conjunction with prone ventilation, complicated by significant airway bleeding, and successfully decannulated after forty-two days, is described. VV ECMO is a resource-intense form of respiratory support. Providing complex therapies such as VV ECMO during a pandemic has its unique challenges. This case report provides a unique insight into the potential clinical sequelae of COVID-19, supported in an intensive care environment which was not resource-limited at the time, and adds to the evolving experience of prolonged VV ECMO support for ARDS with a goal to lung recovery.

Abstract

Nowadays, schizophrenia is treated with atypical antipsychotics that can determine neuroleptic malignant syndrome or rhabdomyolysis appearance. In addition to trauma and muscular hypoxia, there are some drugs and toxins associated with rhabdomyolysis development, among which olanzapine. A case of severe rhabdomyolysis syndrome, with extremely high levels of serum creatine kinase (CK), followed by acute kidney failure, secondary to olanzapine overdose and prolonged immobilization is outlined. Continuous renal replacement therapy was performed, with a slow clearance of serum CK levels. Under supportive therapy, systemic alkalinisation with volume resuscitation and corticotherapy, patient’s general condition was improved, as well as his lower limb paresis. He followed frequent psychiatric evaluations and psychotherapies, before and after being transferred to a medical service. Rhabdomyolysis diagnosis is difficult in mild cases due to non-specific signs and symptoms, but it also has some typical manifestation, generically called “the rhabdomyolysis syndrome triad”. The treatment is usually supportive; renal replacement therapy is required in the presence of acute kidney injury unresponsive to aggressive volume resuscitation. The systemic myoglobin release is responsible for renal injury. Olanzapine muscle toxicity can lead to severe rhabdomyolysis syndrome complicated with acute kidney injury and multiple organ dysfunction syndrome. Rapid identification and aggressive therapeutic management are essential for improving patients’ outcome and prevent the occurrence of irreversible injuries.