Vijay Krishnamoorthy

Preliminary report on cardiac dysfunction after isolated traumatic brain injury.

Objective:The aim of this study was to examine cardiac dysfunction during the first 2 weeks after isolated traumatic brain injury and its association with in-hospital mortality. DesignRetrospective. SettingLevel 1 regional trauma center. PatientsAdult patients with severe traumatic brain injury. Methods:After institutional review board approval, data from adult patients with isolated traumatic brain injury who underwent echocardiography during the first 2 weeks after traumatic brain injury between 2003 and 2010 were examined. Patients with preexisting cardiac disease were excluded. Clinical characteristics and echocardiogram reports were abstracted. Cardiac dysfunction was defined as left ventricular ejection fraction less than 50% or presence of regional wall motion abnormality. Interventions:None. Measurement and Main Results:We examined data from 139 patients with isolated traumatic brain injury who underwent echocardiographic evaluation. Patients were 58 ± 20 years old, 66% were male patients, and 62.6% had subdural hematoma; admission Glasgow Coma Scale score was 3 ± 1 (3–15) and head Abbreviated Injury Scale was 4 ± 1 (2–5). Of this cohort, 22.3% had abnormal echocardiogram: reduced left ventricular ejection fraction was documented in 12% (left ventricular ejection fraction, 43% ± 8%) and 17.5% of patients had a regional wall motion abnormality. Hospital day 1 was the most common day of echocardiographic exam. Abnormal echocardiogram was independently associated with all cause in-hospital mortality (9.6 [2.3–40.2]; p = 0.002). Conclusions:Cardiac dysfunction in the setting of isolated traumatic brain injury occurs and is associated with increased in-hospital mortality. This finding raises the question as to whether there are uncharted opportunities for a more timely recognition of cardiac dysfunction and subsequent optimization of the hemodynamic management of these patients.

Epinephrine Induces Rapid Deterioration in Pulmonary Oxygen Exchange in Intact, Anesthetized Rats A Flow and Pulmonary Capillary Pressure-dependent Phenomenon

Background:Previous studies indicate epinephrine adversely affects arterial oxygenation when administered in a rat model of local anesthetic overdose. The authors tested whether epinephrine alone exerts similar effects in the intact animal. Methods:Anesthetized rats received a single intravenous injection of epinephrine (25, 50, or 100 mcg/kg); matched cohorts were pretreated with phentolamine (100 mcg/kg); n = 5 for each of the six treatment groups. Arterial pressure and blood gases were measured at baseline, 1 and 10 min after epinephrine administration. Pulmonary capillary pressures during epinephrine infusion with normal and increased flows were measured in an isolated lung preparation. Results:Epinephrine injection in the intact animal caused hypoxemia, hypercapnia, and acidosis at all doses. Arterial oxygen tension was reduced within 1 min of injection. Hyperlactatemia occurred by 10 min after 50 and 100 mcg/kg. Rate pressure product was decreased by 10 min after 100 mcg/kg epinephrine. Pretreatment with phentolamine attenuated these effects except at 100 mcg/kg epinephrine. In the isolated lung preparation, epinephrine in combination with increased pulmonary flow increased pulmonary capillary pressure and lung water. Conclusions:Bolus injection of epinephrine in the intact, anesthetized rat impairs pulmonary oxygen exchange within 1 min of treatment. Effects were blunted by &agr;-adrenergic receptor blockade. Edema occurred in the isolated lung above a threshold pulmonary capillary pressure when epinephrine treatment was coupled with an increase in pulmonary flow. These results potentially argue against using traditional doses of epinephrine for resuscitation, particularly in the anesthetized patient.

Airway management in cervical spine injury

To minimize risk of spinal cord injury, airway management providers must understand the anatomic and functional relationship between the airway, cervical column, and spinal cord. Patients with known or suspected cervical spine injury may require emergent intubation for airway protection and ventilatory support or elective intubation for surgery with or without rigid neck stabilization (i.e., halo). To provide safe and efficient care in these patients, practitioners must identify high-risk patients, be comfortable with available methods of airway adjuncts, and know how airway maneuvers, neck stabilization, and positioning affect the cervical spine. This review discusses the risks and benefits of various airway management strategies as well as specific concerns that affect patients with known or suspected cervical spine injury.

Pediatric burn injuries

Pediatric burns comprise a major mechanism of injury, affecting millions of children worldwide, with causes including scald injury, fire injury, and child abuse. Burn injuries tend to be classified based on the total body surface area involved and the depth of injury. Large burn injuries have multisystemic manifestations, including injuries to all major organ systems, requiring close supportive and therapeutic measures. Management of burn injuries requires intensive medical therapy for multi-organ dysfunction/failure, and aggressive surgical therapy to prevent sepsis and secondary complications. In addition, pain management throughout this period is vital. Specialized burn centers, which care for these patients with multidisciplinary teams, may be the best places to treat children with major thermal injuries. This review highlights the major components of burn care, stressing the pathophysiologic consequences of burn injury, circulatory and respiratory care, surgical management, and pain management of these often critically ill patients.

Perioperative estimation of the intracranial pressure using the optic nerve sheath diameter during liver transplantation

An elevation of the intracranial pressure (ICP) secondary to cerebral edema is a major contributor to morbidity and mortality in acute liver failure. In addition, invasive ICP monitoring in this setting is controversial because coagulopathy predisposes patients to hemorrhagic complications. In this case report, we describe the novel use of optic nerve sheath diameter monitoring as a noninvasive modality for checking for acute elevations in ICP in this setting. Because of the merits of rapidly evolving ultrasound technologies, this may serve as a safe method for improving patient care in this setting. Liver Transpl 19:246–249, 2013.

Association between electrocardiographic findings and cardiac dysfunction in adult isolated traumatic brain injury

Introduction: Abnormal electrocardiographic (ECG) findings can be seen in traumatic brain injury (TBI) patients. ECG may be an inexpensive tool to identify patients at high risk for developing cardiac dysfunction after TBI. The aim of this study was to examine abnormal ECG findings after isolated TBI and their association with true cardiac dysfunction, based on echocardiogram. Methods: Data from adult patients with isolated TBI between 2003 and 2010 was retrospectively examined. Inclusion criteria included the presence of a 12-lead ECG within 24 h of admission and a formal echocardiographic examination within 72 h of admission after TBI. Patients with preexisting cardiac disease were excluded. Baseline clinical characteristics, 12-lead ECG, and echocardiogram report were abstracted. Logistic regression was used to identify the relationship of specific ECG abnormalities with cardiac dysfunction. Results: We examined data from 59 patients with isolated TBI who underwent 12-lead ECG and echocardiographic evaluation. In this cohort, 13 (22%) patients had tachycardia (heart rate >100 bpm), 25 (42.4%) patients had a prolonged QTc, and 6 (10.2%) patients had morphologic end-repolarization abnormalities (MERA), with each having an association with abnormal echocardiographic findings: Odds ratios (and 95% confidence intervals) were 4.14 (1.02-17.05), 9.0 (1.74-46.65), and 5.63 (1.96-32.94), respectively. Ischemic-like ECG changes were not associated with echocardiographic abnormalities. Conclusions: Repolarization abnormalities (prolonged QTc and MERA), but not ischemic-like ECG changes, are associated with cardiac dysfunction after isolated TBI. 12-lead ECG may be an inexpensive screening tool to evaluate isolated TBI patients for cardiac dysfunction prior to more expensive or invasive studies.

Cardiac Dysfunction following Brain Death in Children: Prevalence, Normalization and Transplantation

Objectives: Cardiac dysfunction has been reported to occur in as much as 42% of adults with brain death, and may limit cardiac donation after brain death. Knowledge of the prevalence and natural course of cardiac dysfunction after brain death may help to improve screening and transplant practices but adequately sized studies in pediatric brain death are lacking. The aims of our study are to describe the prevalence and course of cardiac dysfunction after pediatric brain death. Design: Cross-sectional study. Setting/Subjects: We examined an organ procurement organization database (Life Center Northwest) of potential pediatric cardiac donors diagnosed with brain death between January 2011 and November 2013. Intervention: Transthoracic echocardiograms were reviewed for cardiac dysfunction (defined as ejection fraction <50% or the presence of regional wall motion abnormalities). Descriptive statistics were used to analyze clinical characteristics and describe longitudinal echocardiogram findings in a subgroup of patients. We examined for heterogeneity between cardiac dysfunction with respect to cause of brain death. Measurement and Main Results: We identified 60 potential pediatric cardiac donors (age ⩽ 18 yr) with at least one transthoracic echocardiogram following brain death. Cardiac dysfunction was present in 23 patients (38%) with brain death. Mean ejection fraction (37.6% vs 62.2%) and proportion of procured hearts (56.5% vs 83.8%) differed significantly between the groups with and without cardiac dysfunction, respectively. Of the 11 subjects with serial transthoracic echocardiogram data, the majority of patients with cardiac dysfunction (73%) improved over time, leading to organ procurement. No heterogeneity between cardiac dysfunction and particular causes of brain death was observed. Conclusion: The frequency of cardiac dysfunction in children with brain death is high. Serial transthoracic echocardiograms in patients with cardiac dysfunction showed improvement of cardiac function in most patients, suggesting that initial decisions to procure should not solely depend on the initial transthoracic echocardiogram examination results.

Traumatic Brain Injury in the Elderly: Burden, Risk Factors, and Prevention

Traumatic brain injury (TBI) is a major public health problem, affecting millions of people each year worldwide. Elderly patients are at particularly high risk after sustaining a TBI due to higher degrees of mortality and functional disability compared with younger patients. In addition, the causative mechanisms of TBI in the elderly are shifting from motor vehicle collisions to falls. In this article, we will review the risk factors and mechanisms that predispose elderly patients to sustain a TBI. We will conclude by using a “Haddons Matrix” approach to review current evidence-based prevention strategies directed at reducing the burden of TBI in the elderly.

Myocardial dysfunction in acute traumatic brain injury relieved by surgical decompression.

Traumatic brain injury (TBI) is a major public health issue and is a leading cause of death in North America. After a primary TBI, secondary brain insults can predispose patients to a worse outcome. One of the earliest secondary insults encountered during the perioperative period is hypotension, which has been directly linked to both mortality and poor disposition after TBI. Despite this, it has been shown that hypotension commonly occurs during surgery for TBI. We present a case of intraoperative hypotension during surgery for TBI, where the use of transthoracic echocardiography had significant diagnostic and therapeutic implications for the management of our patient. We then discuss the issue of cardiac dysfunction after brain injury and the implications that echocardiography may have in the management of this vulnerable patient population.

Patent foramen ovale and intracardiac thrombus identified by transesophageal echocardiography during liver transplantation

Vascular anastomosis was completed, and the vascular crossclamps were removed to establish hepatic reperfusion (stage III) after only 24 minutes of warm ischemia time and 261 minutes of cold ischemia time. Reperfusion during the first minute was tolerated well, with a BP of 110/60 mmHg, HR of 110 beats/min, SaO2 of 100% on 100% FIO2, systolic/diastolic PAP of 30/18 mmHg, CVP of 10 mmHg, CI of 5.5 L/min/m2, and SvO2 of 81%. Five minutes after reperfusion, the patient’s BP suddenly decreased to 81/42 mmHg with an associated HR of 58 beats/min. A TEE revealed a large free-floating thrombus in the right atrium. The thrombus started in the inferior vena cava (IVC) (Video 2), extended into the PFO (Video 3), and was partially obstructing the tricuspid valve and right ventricular inflow (Video 4). The thrombus position was highly concerning given that a massive embolus could occur. If the thrombus further migrated into the left atrium through the PFO (Fig 2), then the potential of a systemic embolus existed. If the thrombus migrated into the right ventricle, then the potential of a massive pulmonary embolus existed. The surgeon was notified, and suction of the venous anastomosis site was initiated in order to decrease the right atrial pressure. The BP was increased with intravenous epinephrine, 50 g, in order to increase the left atrial pressure, with the aim to keep a left-toright shunt through the PFO and maintain the thrombus in the right atrium. During this time, unfractionated heparin (2,000 U 2 boluses) was given at 5-minute intervals in order to stabilize the clot formation, which resulted in rapid resolution of the clot from the right ventricle inflow only 10 minutes after clot detection. No clinical signs of pulmonary embolism were noted because PAPs remained within normal limits with no right ventricular dysfunction and no wall motion abnormality on TEE.