Case Reports in Critical Care最新文献

HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome is a rare but serious complication of pregnancy characterized by hemolytic anemia, elevated liver enzymes, and thrombocytopenia. It occurs in <1% of all pregnancies with 70% of cases developing before delivery, the majority occurring between the 27^th and 37^th weeks of gestation. Respiratory failure seen in HELLP syndrome clinically and radiographically appears similar to acute respiratory distress syndrome (ARDS), with presence of bilateral pulmonary opacities on imaging as well as persistent hypoxemia requiring elevated ventilator requirements. It is seen to complicate 3-10% of cases of HELLP syndrome. Pulmonary complications are theorized to occur as sequelae of the proinflammatory state induced by HELLP syndrome with endothelial dysfunction and subsequent microangiopathic hemolysis and thrombocytopenia. A robust cytokine inflammatory response similar to ARDS is seen, resulting in noncardiogenic pulmonary edema due to vasoplegia and capillary leak syndrome. We present a case of a 27-year-old uniparous female with a term pregnancy complicated by HELLP syndrome who developed respiratory failure requiring mechanical ventilation. Early CRRT and nitric oxide therapy were initiated, with the patient experiencing clinical and radiological improvement of respiratory function within 48 hours. We document the novel treatment of our patient's acute respiratory failure with CRRT and nitric oxide and delve into the literature regarding its use in acute respiratory failure and ARDS in association with HELLP syndrome.

Judicious balance of fluids is needed for optimal management of acute respiratory distress syndrome (ARDS). Achieving optimal fluid balance is difficult in patients with disorders of fluid homeostasis such as diabetes insipidus (DI). There is little data on the use of Furosemide to aid in balancing fluid and electrolytes in patients with DI. Here, we present a critically ill 11-year-old female with developmental delay, septo-optic dysplasia, central DI, and respiratory failure secondary to COVID-19 ARDS. She required careful titration of a Vasopressin infusion in addition to IV Furosemide for successful management of fluid and electrolyte derangements. On admission, she demonstrated high-volume urine output with mild hypernatremia (serum sodium 156 mmol/L). Despite her maximum Vasopressin infusion rate of 8 mU/kg/hr, by day two of admission, she voided a total of 4 L resulting in severe hypernatremia (serum sodium 171 mmol/L). With continually high Vasopressin infusion rates, her overall fluid balance became increasingly net positive, although her hypernatremia persisted. Her ARDS continued to worsen. After 48 hours of the addition of intermittent Furosemide, successful diuresis along with resolution of hypernatremia was achieved. The combination of IV Furosemide with Vasopressin infusion resulted in tailored diuresis and more controlled titration of serum sodium levels than adjustment in Vasopressin and fluids alone. These results are in contradistinction to the published literature, which focuses on the use of thiazide diuretics in managing DI. This experience highlights the potential for loop diuretics to aid in establishing a desired fluid and electrolyte status in managing patients with both DI and ARDS.

Transsphenoidal surgery (TSS) is a frequently used technique to remove pituitary adenomas. Rare complications of TSS include development of postoperative pneumocephalus. Many patients undergoing TSS also suffer from obstructive sleep apnea (OSA) and thus require positive pressure ventilation. The exact timing of when to safely reintroduce the CPAP machine in this subset of patients is presently not exactly known but is most often cited as being two to four weeks postoperatively. In this case, we describe the story of a 69-year-old female who underwent TSS for a nonsecreting pituitary adenoma in April 2012 and went on to develop pneumocephalus five weeks postoperatively after reintroduction of her CPAP machine. This is the latest presentation of pneumocephalus after reintroduction of CPAP documented in present literature. The case reopens the debate as to how many weeks postoperatively positive pressure ventilation should be withheld to prevent the development of pneumocephalus in patients having undergone TSS with simultaneous OSA.

Background: Eptifibatide is a glycoprotein IIb/IIIa (GP IIb/IIIa) receptor inhibitor which prevents platelet activation. The mechanism in which eptifibatide causes profound thrombocytopenia is poorly understood. One hypothesis suggests antibody-dependent pathways which cause thrombocytopenia upon subsequent reexposure to eptifibatide. This case reports acute profound thrombocytopenia (platelets < 20 × 10³/mm³) within 24 hours of administration. Alveolar hemorrhage occurred during a second eptifibatide infusion 5 days after initial asymptomatic eptifibatide treatment. Case Presentation. A 50-year-old male presenting with a STEMI was treated with eptifibatide during cardiac catheterization. Twelve hours posttreatment, the patient encountered profound thrombocytopenia and hemoptysis. The patient was briefly intubated for airway protection. The patient was stabilized after receiving platelet transfusion and fully recovered.

Conclusion: This is one of several cases reported on eptifibatide causing acute profound thrombocytopenia and subsequent alveolar hemorrhage. This case supports the theory in which antibodies contribute to eptifibatide-induced thrombocytopenia.

Acetaminophen overdose is one of the most common causes of acute hepatic failure in the developed world. There is strong evidence for N-acetylcysteine (NAC) as a safe and effective antidote for acetaminophen toxicity. However, there is less clarity in the management of massive overdoses (acute, single ingestions > 500 mg/kg with 4-hour equivalent concentrations ~6000 μmol/L) which are often associated with metabolic acidosis and multiorgan dysfunction. In such ingestions, the role of adjuvant treatments such as fomepizole and extracorporeal removal is unclear. We present a case of a 20-year-old female presenting with an acute ingestion of over 120 grams (1764.7 mg/kg) and an acetaminophen concentration of 5880 μmol/L who developed refractory shock, decreased level of consciousness, and metabolic acidosis requiring mechanical ventilation and vasopressor support. She was treated with gastric decontamination with activated charcoal, IV NAC, fomepizole, and hemodialysis. The patient had complete clearance of acetaminophen by 32 hours after presentation and normalization of her acid base and hemodynamic status without any organ failure. This case highlights the potential benefit of a triple strategy of NAC, fomepizole, and early hemodialysis in massive acetaminophen overdose, potentially sparing complications of prolonged intubation and ICU hospitalization.

Veno-venous extracorporeal membrane oxygenation (V-V ECMO) may be required to treat critically ill patients with COVID-19-associated severe acute respiratory distress syndrome (ARDS). We report the case of a 43-year-old peripartum patient, who underwent two sequential V-V ECMO runs. The first extracorporeal support was established for COVID-19 ARDS, as characterized by severe hypoxemia and hypercapnia (arterial partial pressure of oxygen to inspired oxygen fraction ratio 85 mmHg and arterial partial pressure of carbon dioxide 95 mmHg) and reduction of respiratory system static compliance to 25 mL/cmH₂O, unresponsive to mechanical ventilation and prone positioning. After 22 days of lung rest, V-V ECMO was successfully removed and ventilator weaning initiated. A second V-V ECMO was required 7 days later, because of newly onset ARDS due to Pseudomonas aeruginosa ventilator-associated pneumonia. The second V-V ECMO run lasted 12 days. During both V-V ECMO runs, anticoagulation and ventilator settings were titrated through bedside thromboelastometry and electrical impedance tomography, respectively, without major complications. The patient was successfully decannulated, weaned from mechanical ventilation, and finally discharged home without oxygen therapy. At one-month follow-up, she showed good general conditions and no sign of respiratory failure.

Acute respiratory distress syndrome (ARDS) due to COVID-19 leads to a high rate of mortality in the intensive care unit (ICU). A lung-protective mechanical ventilation strategy using low tidal volumes is a cornerstone to management, but uncontrolled hypercapnia is a life-threatening consequence among severe cases. A mechanism to prevent progressive hypercapnia may offset hemodynamic instability among patients who develop hypercapnia. We present the case of a woman in her mid-60's with severe acute hypercapnic respiratory failure secondary to COVID-19 pneumonia who was successfully treated with early implementation of lung-protective ventilation facilitated by extracorporeal carbon dioxide removal (ECCO₂R). This patient's multiple comorbid conditions included obesity, hypertension, type 2 diabetes mellitus, and hypercholesterolemia. On her fifth day of admission at the referring hospital, her worsening hypoxemia prompted endotracheal intubation during which she developed pneumothorax. She was transferred to our institution for advanced care where upon arrival, she had profound hypercapnia and respiratory acidosis. She met the criteria for treatment with an investigational ECCO₂R device (Hemolung Respiratory Assist System) available through FDA Emergency Use Authorization. ECCO₂R is similar to extracorporeal membrane oxygenation (ECMO) but operates at much lower blood flows (350-550 mL/min) through a smaller 15.5 French central venous catheter. Standard heparinization was provided intravenously to achieve appropriate levels of anticoagulation during ECCO₂R therapy. Unlike ECMO, ECCO₂R does not provide clinically meaningful oxygenation but is simpler to implement and manage. The use of ECCO₂R successfully corrected and controlled the patient's hypercapnia and acidosis and enabled meaningful reductions in ventilator tidal volumes, respiratory rates, and mean airway pressures. The patient was weaned from ECCO₂R after 17 days and from mechanical ventilation 10 days later. With low tidal volume ventilation facilitated by expeditious implementation of ECCO₂R, the patient survived to discharge despite her many risk factors for a poor outcome and an extended duration of invasive mechanical ventilation.

Objectives: To report a case of povidone-iodine (PVP-I, Iso-Betadine®) disinfection of lower leg fasciotomy wounds resulting in iodide absorption and possibly contributing to hypothyroidism and prolonged kidney injury.

Design: Case report. Setting. Pediatric intensive care unit (PICU), university hospital. Patients. A 13-year-old patient presenting with prolonged oligoanuric kidney failure and unexplained primary hypothyroidism three weeks after severe abdominal sepsis with multiple organ dysfunction and major rhabdomyolysis due to bilateral lower leg compartment syndrome, necessitating moderate size fasciotomies, disinfected daily with PVP-I. Interventions. Interruption of PVP-I exposure and initiation of thyroid hormone substitution. Measurements and Main Results. Hypothyroidism was revealed during diagnostic work-up for persistent hypertriglyceridemia. Thyroxine (T4) (4.0 mg/L) and tri-iodothyronine (T3) (64 ng/L) were moderately low, yet thyroid stimulating hormone (TSH) (16.8 mIU/L) was fourfold the maximal normal range value. This pattern, atypical for prolonged critical illness-related hypothyroidism, prompted interruption of PVP-I exposure and initiation of thyroid hormone substitution. Urinary production and creatinine clearance recovered during the following days, and one week later, intermittent renal replacement therapy could be terminated, suggesting that PVP-I toxicity and/or hypothyroidism may have contributed to the persistent renal failure three weeks after resolved septic shock and rhabdomyolysis. Elevated serum and urinary anion gap normalized simultaneously, but this evolution of rather nonspecific indices could be multifactorial.

Conclusion: PVP-I is a commonly used broad-spectrum antimicrobial agent for prevention and treatment of wound infections. Toxic complications due to PVP-I absorption, after disinfection of extended thermal injuries larger than 20% of the body surface, have been described. In critically ill children, however, toxic effects of PVP-I may occur due to repeated disinfection of less extended wounds. Proposed screening strategies include: monitoring of the volumes of PVP-I applied daily; of the thyroid function, the serum, and/or urinary anion gap and the urinary iodide concentrations. These strategies, however, remain to be validated. This case report should be a wake-up call for daily integration of wound management in the clinical evaluation of critically ill patients.

Evidence exists for the use of high-flow nasal oxygen (HFNO) in the general critical care population for acute hypoxemic respiratory failure. There is discord between guidelines for hypoxemia management in COVID-19. Both noninvasive management and intubation present risk to patients and staff and potentially overwhelm hospital mechanical ventilator capacity. The use of HFNO has been particularly controversial in the UK, with oxygen infrastructure failure. We discuss our experience of managing COVID-19 with HFNO and awake self-prone positioning. We focus upon the less-usual case of an eighteen-year-old female to illustrate the type of patient where HFNO may be used when perhaps earlier intubation once was. It is important to consider the wider implications of intubation. We have used HFNO as a bridge to intubation or as definitive management. As we await clinical trial evidence, HFNO with self-prone positioning has a role in COVID-19 for certain patients. Response parameters must be set and reviewed, oxygen infrastructure considered, and potential staff droplet exposure minimised.

Flecainide is a class 1C antiarrhythmic with a narrow therapeutic window and thereby a high-risk medication for causing acute toxicity. Dysrhythmias secondary to flecainide ingestion are often refractory to antiarrhythmics and cardioversion, and patients commonly require extracorporeal support. We review the successful resuscitation of two brothers aged 2 and 4 who presented two years apart with unstable wide-complex tachyarrhythmia suspicious for severe flecainide toxicity. Each patient received sodium bicarbonate and 20% intravenous lipid emulsion with a full recovery. While extracorporeal support is often required following flecainide ingestion, we present two cases where it was avoided due to aggressive multimodal management with sodium bicarbonate, electrolyte repletion, and 20% intravenous lipid emulsion. In addition, avoidance of agitation-induced tachycardia may be beneficial.