Thrombocytopenia is a common entity seen in ICU patients and is associated with increased morbidity such as bleeding and transfusions, and mortality in ICU patients. Various mechanisms such as decreased platelet production, sequestration, destruction, consumption, and sometimes a combination of these factors contribute to thrombocytopenia. An understanding of the mechanism is essential to diagnose the cause of thrombocytopenia and to help provide appropriate management. The management strategies are aimed at treating the underlying disorder, such as platelet transfusion to treat complications like bleeding. Several studies have aimed to provide the threshold for platelet transfusions in various clinical settings and recommend a conservative approach in the appropriate scenario. In this review, we discuss various pathophysiological mechanisms of thrombocytopenia and the diverse scenarios of thrombocytopenia encountered in the ICU setting to shed light on the varied thresholds for platelet transfusion, alternative agents to platelet transfusion, and future directions for the implementation of thromboelastography (TEG) in multiple clinical scenarios to assist in the administration of appropriate blood products to correct coagulopathy.
Pleural space infections have been described since the time of Hippocrates and to this day remains a significant pathology. Every year in the USA approximately there are one million hospital admissions for pneumonia with 20%-40% associated with some form of pleural space infections leading to pleural effusions with increased morbidity and mortality. Often, management of these effusions mandate combination of medical treatment and surgical drainage with debridement and decortication. There has been a lot of ongoing research regarding the safety and efficacy of intrapleural fibrinolytics in the management of complicated pleural effusions and empyema. Till this day, areas of debate and controversies exist among clinicians treating pleural space infection. Empyema is historically considered a surgical disease. There have been societies and guidelines for the management of infected parapneumonic effusions with antibiotics and chest tube drainage as an initial empiric treatment modality. With the advances in the use of Intrapleural fibrinolytics and minimally invasive procedures such as video-assisted thoracoscopic surgery (VATS), empyema a surgical disease is now more favoring medical management. Surgical option, such as open thoracotomy, is reserved for patients who failed conservative management and chronic empyema. The aim of this comprehensive review is to shed light on the evolution of various management strategies from the era of Hippocrates to current day practice and how there continues to be a paradigm shift in treating empyema as a surgical condition to a medical disease.
INTRODUCTION: Botulism is a rare, but potentially life-threatening neuroparalytic syndrome that can be caused by accidental (Foodborne or wound infection) or Iatrogenic exposure to botulinum toxins. Iatrogenic causes of botulism have been reported rarely in patients who have received botulinum toxin for cosmetic indications. Botulinum toxins work by blocking Acetylcholine release causing muscle relaxation. Serotypes A to G has been identified with type A causing the most severe syndrome. Botox (onabotulinum toxin A), used for cosmetic purposes, including but not limited to cervical dystonia, hyperhidrosis, upper and lower limb spasticity, and urinary incontinence. If botulinum neurotoxin enters the vascular system and is transported to peripheral cholinergic nerve terminals, including neuromuscular junctions, postganglionic parasympathetic nerve endings, and peripheral ganglia, it can lead to loss of strength, double vision, drooping eyelids, hoarseness, loss of bladder control, trouble breathing.
Case series Patients: Male, 71-year-old • Female, 58-year-old Final Diagnosis: Pulmonary barotrauma Symptoms: Pneumomediastinum Medication: — Clinical Procedure: Chest tube Specialty: Critical Care Medicine Objective: Unusual clinical course Background: Invasive mechanical ventilation can cause pulmonary barotrauma due to elevated transpulmonary pressure and alveolar rupture. A significant proportion of COVID-19 patients with acute respiratory distress syndrome (ARDS) will require mechanical ventilation. We present 2 interesting cases that demonstrate the possibility of COVID-19-associated ARDS manifesting with pulmonary barotrauma at acceptable ventilatory pressures. Case Reports: The first patient was a 71-year-old man who was intubated and placed on mechanical ventilation due to hypoxemic respiratory failure from SARS-CoV-2 infection. His partial pressure of O2 to fraction of inspired oxygen ratio (PaO2/FiO2) was 156. He developed subcutaneous emphysema (SE) and pneumomediastinum on day 5 of mechanical ventilation at ventilatory settings of positive end-expiratory pressure (PEEP) ≤15 cmH 2 O, plateau pressure (Pplat) ≤25 cmH 2 O and pulmonary inspiratory pressure (PIP) ≤30 cmH 2 O. He was managed with ‘blow-hole’ incisions, with subsequent clinical resolution of subcutaneous emphysema. The second patient was a 58-year-old woman who was also mechanically ventilated due to hypoxemic respiratory failure from COVID-19, with PaO2/FiO2 of 81. She developed extensive SE with pneumomediastinum and pneumothorax while on mechanical ventilation settings PEEP 13 cmH 2 O and PIP 28 cmH 2 O, Pplat 18 cmH 2 O, and FiO2 90%. SE was managed with blow-hole incisions and pneumothorax with chest tube. Conclusions: Clinicians should be aware of pulmonary barotrauma as a possible complication of COVID-19 pulmonary disease, even at low ventilatory pressures.
Hyperammonemia is a metabolic disturbance characterized by excess ammonia in the blood and a lifethreatening condition that can affect patients of any age. It is a dangerous condition that may lead to cerebral edema, brain injury, and death. It is commonly associated with acute or chronic liver failure with or without hepatic encephalopathy, inborn errors of metabolism, upper gastrointestinal bleeding, and non-hepatic causes include chemotherapy, valproic acid, ureterosigmoidostomy, UTIs. Elevations of ammonia in plasma indicate its increased production and/or decreased detoxification.
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