Craig Ainsworth

Severe Hemolytic Anemia Post–Renal Transplantation Produced by Donor Anti-D Passenger Lymphocytes: Case Report and Literature Review

The passenger lymphocyte syndrome (PLS), often associated with immune-mediated hemolytic anemia after solid organ and hematopoietic stem cell transplantation, is the result of concomitant transplantation of donor lymphocytes along with the donor allograft. Antibodies directed against recipient red blood cells (RBCs) are frequently found in ABO-mismatched solid organ transplants; however, passenger lymphocyte-mediated hemolysis due to Rh-incompatible antibodies has only rarely been reported. In this report, we present a case of severe hemolytic anemia related to the PLS in an ABO-matched renal allograft recipient. The recipients blood type was A Rh(D) positive; and the donor, who had been previously alloimmunized, was A Rh(D) negative. The renal allograft recipients hemoglobin abruptly decreased on postoperative day 12 in the setting of a newly positive direct antiglobulin test and anti-D antibodies in the plasma. The patient required intermittent RBC transfusions for ongoing hemolysis during the first 6 months post-renal transplant. Of all reported cases of anti-D-mediated PLS, our patient would seem to have been one of the most severe, as indicated by a nadir hemoglobin of 41 g/L and the need for 23 U of transfused RBCs. A hemolytic anemia occurring after organ transplantation should raise the possibility of donor-derived antibodies directed against the recipient RBCs. Passenger lymphocyte syndrome-associated hemolysis is occasionally severe as in our case, but can be effectively treated with compatible RBC transfusions.

Canadian recommendations for critical care ultrasound training and competency

OBJECTIVE To achieve national consensus on standards of training, quality assurance and maintenance of competence for critical care ultrasound for intensivists and critical care trainees in Canada using recently published international training statements. DATA SOURCES Existing internationally endorsed guidelines and expert opinion. DATA SYNTHESIS In November 2013, a day-long consensus meeting was held with 15 Canadian experts in critical care ultrasound in which essential topics relevant to training ultrasound were discussed. CONCLUSIONS Consensus was achieved to direct training curriculum, oversight, quality assurance and maintenance of competence for critical care ultrasound. In providing the first national guideline of its kind, these Canadian recommendations may also serve as a model of critical care ultrasound dissemination for other countries.

Treatment of Unicentric Castleman Disease With Neoadjuvant Rituximab

Angiofollicular lymph node hyperplasia, known more commonly as Castleman disease, is a rare lymphoproliferative disorder. Castleman disease has two distinct clinical manifestations described as unicentric and multicentric disease. These presentations have distinct treatment algorithms and portend very different prognoses. Standard treatment of unicentric disease is complete surgical resection, which confers a cure rate approaching 100%. To our knowledge, this case report is the first to describe the use of neoadjuvant rituximab in the treatment of unicentric Castleman disease to enable a less morbid surgical resection. Given the vascularity of the tumor, proximity to the pulmonary artery and superior vena cava, and possible intimate association with the lung parenchyma, the tumor was treated preoperatively with rituximab, an anti-CD20 monoclonal antibody, at doses of 375 mg/m² weekly for 4 weeks. Rituximab therapy successfully decreased the diameter of the tumor from 4.79 cm×2.67 cm to 2.8 cm×1.5 cm, as confirmed by CT imaging. Postoperative surgical pathology confirmed the diagnosis of Castleman disease, hyaline vascular type, with negative margins. Notably, the lymph node tissue in the rituximab-treated specimen demonstrated reduced mantle zone thickness, decreased size of follicles, and increased hyalinization of vessels. Rituximab shows promise in neoadjuvant treatment of unresectable or partially resectable unicentric Castleman disease.

Echo-Guided Pericardiocentesis Let the Bubbles Show the Way

A 75-year-old man with coronary artery disease, atrial fibrillation, sick sinus syndrome with permanent pacemaker, hypertension, dyslipidemia, and previous exertional dyspnea related to moderately severe mitral regurgitation from myxomatous degeneration and bileaflet prolapse presented with progressively worsening dyspnea several weeks after undergoing successful mitral and tricuspid valve repair with insertion of annuloplasty rings in addition to 2-vessel coronary artery bypass surgery. On presentation to the hospital he was found to have dyspnea at rest, hypotension, and jugular venous distension. A transthoracic echocardiogram demonstrated normal left ventricular function, no significant valvular stenosis, or regurgitation and a moderate sized pericardial effusion measuring 1.4 cm anteriorly and 2.7 cm posteriorly (Figure A through C). Significant inferior vena cava dilatation was noted, but no convincing chamber collapse to suggest overt cardiac tamponade. His symptoms persisted with no alternate cause …

From Coronary Care Units to Cardiac Intensive Care Units: Recommendations for Organizational, Staffing, and Educational Transformation

Medical care in Canadian cardiac units has changed considerably over the past 3 decades in response to an increasingly complex and diverse patient population admitted with acute cardiac pathology. To maintain the highest level of care for these patients, there is a pressing need to evolve traditional coronary care units into contemporary cardiac intensive care units. In this article we aim to highlight the current variations in Canadian units, develop approaches to overcome logistical and infrastructural obstacles, and propose staffing and training recommendations that would allow for the establishment of contemporary cardiac intensive care units.

A Bloody Mass Rare Cardiac Tumor as a Cause of Symptomatic Ventricular Arrhythmias

An active, physically fit, and previously healthy 23-year-old man is referred by his family physician to a cardiology clinic with a several-month history of progressively worsening episodes of palpitations associated with dyspnea. He reports experiencing brief episodes almost hourly and describes the palpitations as being extremely rapid and the rhythm as regular. Dr Salehian : Palpitations as a chief complaint are a common issue routinely assessed by family physicians, general internists, emergency department physicians, and cardiologists. The differential diagnosis in such patients is broad and often not related to a primary cardiac issue or arrhythmia. Broadly, symptoms of palpitations may be related to cardiac arrhythmia or structural heart disease, medications, recreational drugs and alcohol, metabolic disorders, high output states, or psychiatric conditions. To help to determine the etiology of the patients symptoms, a thorough history, physical examination, and basic laboratory investigations are necessary to help to determine which further investigations are required. The patient reports mild dyspnea with the episodes but denies associated syncope or presyncope, chest discomfort, nausea, or vomiting. The palpitations are not precipitated by exertion, and there are no other identifiable aggravating factors. He is unaware of any physical activity limitations, exertional symptoms, or features suggestive of congestive heart failure. There is no drug or alcohol use and absence of a family history of early coronary artery disease, congenital heart disease, dysrhythmia, or sudden cardiac death. He also denies recent infectious symptoms. On physical examination, he is afebrile, with a blood pressure of 116/72 mm Hg, heart rate of 68 bpm, and respiratory rate of 14 breaths per minute. There is no adenopathy noted, and the jugular venous pressure is not elevated. Carotid upstroke is normal without any bruits. On cardiac examination, apical impulse is not easily palpable, and no obvious heaves or thrills are felt. On …

Adherence to advanced cardiovascular life support (ACLS) guidelines during in-hospital cardiac arrest is associated with improved outcomes

AIM OF THE STUDY Identifying modifiable factors associated with survival following in-hospital cardiac arrest is crucial. The purpose of this study was to determine the extent to which adherence to the 2010 American Heart Association (AHA) Advanced Cardiac Life Support (ACLS) guidelines in their entirety affects patient outcomes. In addition, we explored the role of code leader training level on patient outcomes. METHODS We conducted a retrospective review of records for cardiac arrests that occurred on hospital wards and were run by the hospital code team, at three tertiary care centres over 2 to 4 years. Deviations from the ACLS guidelines were quantified using a standardized checklist. Primary outcomes included return of spontaneous circulation (ROSC) and survival to hospital discharge. RESULTS Of 160 resuscitation events, ROSC was achieved in 75 events (46.9%) and survival to hospital discharge in 20 patients (13.1%). On average, there were 2.3 deviations from ACLS guidelines during events that led to ROSC and 3.9 deviations during events that did not lead to ROSC (p < 0.0001). There were fewer deviations during events that led to survival to hospital discharge (2.1) compared to those where the patient did not survive to hospital discharge (3.1; p = 0.016). Code leader training level was not associated with patient outcomes. Multivariable logistic regression analysis confirmed an association between deviations from ACLS guidelines and ROSC, but not for survival to hospital discharge. The latter finding may reflect a very low survival rate. CONCLUSION We found that higher numbers of deviations from ACLS guidelines were associated with a lower likelihood of ROSC and survival to hospital discharge. These findings emphasize the importance of adherence to ACLS guidelines and the need for training healthcare personnel in resuscitation guidelines in order to improve outcomes for victims of in-hospital cardiac arrest.

The potential role of a turbidimetric heart-type fatty acid-binding protein assay to aid in the interpretation of persistently elevated, non-changing, cardiac troponin I concentrations

BACKGROUND Elevated and non-changing high-sensitivity cardiac troponin (hs-cTn) concentrations may suggest a process other than acute injury, possibly due to chronic condition(s) causing the elevation, an analytical error/interference or the formation of macrocomplexes. Heart-type fatty acid binding protein (H-FABP) might be useful in this setting to identify the etiology of abnormally high and non-changing cTn concentrations which could aid clinical decision making in the hospital setting. METHODS We analytically validated the H-FABP assay (Randox) on the Abbott ARICHTECTc8000 platform, testing imprecision, linearity, stability, and matrix comparison. Over the 2-month analytical validation; EDTA plasma samples from patients with a hospital visit with persistently elevated and stable cTnI concentrations (Abbott hs-cTnI≥52 ng/L or 2x99th percentile upper limit of normal (ULN = 26 ng/L) with change between results <20%) were collected and frozen (-20 °C). These samples were tested with the H-FABP assay, polyethylene glycol (PEG) precipitation, with the lowest estimated glomerular filtration rate (eGRF) during the hospital visit also obtained from these patients. RESULTS The H-FABP assay was linear, with concentrations stable after 4 freeze/thaw cycles, up to 150 h at room temperature, and comparable between lithium heparin and EDTA plasma. During the validation there were 6 patients with eGFR ≥60 ml/min/1.73m2 identified (total population screened n = 917) with high and non-changing hs-cTnI concentrations. All 6 patients had H-FABP<2xULN; with 3 patients having a macrocomplex and a final diagnosis of not ACS. CONCLUSION Testing of H-FABP in patients with an eGFR≥60 ml/min/1.73m2 with persistently high and stable cTn elevations may help to confirm prior cardiac injury or the presence of macrocomplexes as the source of these elevations.

13: THE EFFECT OF DEVIATIONS FROM ACLS GUIDELINES ON OUTCOMES OF IN-HOSPITAL CARDIAC ARREST

Crit Care Med 2015 • Volume 43 • Number 12 (Suppl.) arterial pressure (MAP), prevented brain edema, and limited intracranial pressure (ICP) during combined TBI+HS resuscitation vs lactated Ringers (LR). Definitive studies to define the optimal dose of PNPH are needed for clinical trial design. Hypothesis: Volumes of PNPH as small as 5 mL/kg are equally effective as 20 ml/kg in TBI resuscitation. Methods: Mice (n=10/group) underwent controlled cortical impact followed by a 35-min severe HS. Mice then were randomized to 3 resuscitation groups (initial dose of PNPH 5mL/kg, PNPH 20mL/kg, or LR 20mL/kg followed by LR boluses every 5min for MAP<70 during a 90 min “prehospital” phase). Lastly, they received reinfusion of shed blood during a 15-min “hospital” phase. ICP and MAP were monitored and % brain water (% BW) in injured and contralateral hemispheres determined at 24h (wet-dry weight). Results: The amount of fluid needed differed between the 5, 20 and LR groups (56 ± 3, 24 ± 3, and 184 ± 4 mL/ kg, all comparisons p<0.05). Repeated measures [RM]ANOVA for MAP showed a treatment effect vs LR at both doses (p<0.01) and 20 >5 (p<0.05). At end of the prehospital phase MAP was 66.7 ± 2.4, 68.6 ± 2.6 vs 57.2 ± 2.2 mmHg, in 5, 20 and LR. RMANOVA for ICP did not differ between groups (p=0.2); there was a trend for reduced ICP in both PNPH groups vs LR (9.5 ± 1.0, 10.2 ± 1.0 vs 14.3 ± 2.0 mmHg, at end of pre-hospital phase). Mice resuscitated with 5 or 20mL/kg of PNPH 20mL/ kg showed reduced %BW vs LR in both ipsilateral (79.91 ± 0.20 and 79.96 ± 0.27 vs 80.83 ± 0.30, p=0.03) and contralateral (78.19 ± 0.11 and 78.08 ± 0.13 vs 78.79 ± 0.15, p<0.01) hemispheres. Conclusions: PNPH equally attenuated brain edema at 5 or 20mL/kg doses. Both doses also improved MAP and greatly reduced fluid requirements. Doses of PNPH as low as 5 mL/kg may be useful in TBI resuscitation. Support:U44NS070324, CEEDII ICRE.