Unexplained Hypotension Research Articles

Keeping Patients Safe During Intrahospital Transport

Keeping Patients Safe During Intrahospital Transport

Hemodynamic Instability due to Adrenal Insufficiency after Open Heart Surgery

Unexplained hypotension during a stay in the ICU is not uncommon in patients who underwent major surgery such as open heart surgery. When the cardiac output of patients is low, the heart may be the origin of this problem. If the heart function is normal, then we have to consider adrenal insufficiency as a possible cause of this hypotension. Adrenal insufficiency is a rare condition in the general population, yet patients who are under a stressful condition might experience adrenal insufficiency more frequently. We report here on a case of a patient who was in an unstable postoperative state with adrenal insufficiency after surgery and the patient dramatically recovered after the replacement of hydrocortisone. (Korean J Thorac Cardiovasc Surg 2010;43:191-193)

Traumatic adrenal gland injury: epidemiology and outcomes in a major Australian trauma center.

Adrenal gland injury (ADGI) is quite rare and mostly associated with other organ injuries secondary to blunt thoracoabdominal trauma. Bilateral ADGI has severe consequences if not discovered in the treatment course of trauma victims. To review our experience of management of ADGI, epidemiology, and outcomes in a major Australian trauma institute. A retrospective analysis of all patients presenting with thoracoabdominal trauma to the Alfred Hospital who had been diagnosed with adrenal gland injury between July 2001 and July 2007. Of 3,921 patients with blunt thoracoabdominal injuries, 2.4% were identified with blunt ADGI (70 males and 26 women, age range 15-85years). Right adrenal injuries occurred in 72.9%, left adrenal injuries in 22.9%, and bilateral ADGI in 4.2%. Computed tomography (CT) scan findings revealed 82.2% of acute injuries to be hyperdense hematoma expanding and distorting the adrenal gland. Periadrenal stranding and hemorrhagic changes around the adrenal limbs were seen in 12.5%. Oval or round lesions were seen in 3.1%. Surgery was performed in 25% of the study group for associated thoracoabdominal injuries. Patients with left adrenal gland injury had higher rates of mortality and morbidity, and length of stay. ADGI is being increasingly recognized with the widespread use of CT scan in the evaluation of multitrauma patients. ADGI is usually self-limiting and typically managed nonoperatively. Acute adrenal insufficiency should be considered and investigated in case of unexplained hypotension in uni- or bilateral ADGI.

Survival of a Patient With Blunt Traumatic Biatrial Rupture

Cardiac rupture after blunt injury of the chest is uncommon and usually fatal. The incidence of biatrial cardiac rupture is rarer and more likely to be lethal. We report a case of biatrial multiple lacerations following blunt chest injury. At referral, the chest film showed left side massive hemothorax. A chest tube was inserted and primary resuscitation was carried out. The patient's vital signs became stable and he was transferred to our hospital for further management. The time from the injury occurring and the patient arriving at our hospital was 117 minutes. Unexplained hypotension was noted on arrival and bedside ultrasonography revealed cardiac tamponade. After emergent pericardiocentesis, the patient's hemodynamics stabilized. Emergency surgery was performed and the patient was discharged without any sequelae. We successfully managed this case through a high index of suspicion, aggressive investigation, and prompt exploration.

Assessment of cardiac injury in patients with blunt chest trauma.

There has been difficulty in the appropriate determination of blunt cardiac injury (BCI) related to blunt thoracic trauma (BTT). The aim of this study is to assess BCI and the effectiveness of diagnostic tests in BTT in patients admitted to the emergency department (ED). Eighty-eight patients with suspected myocardial injury in BTT were enrolled. The diagnostic criteria for BCI were: elevation of troponinI, arrhythmia requiring treatment, unexplained low voltage on electrocardiography (ECG), unexplained hypotension requiring vasopressor, cardiogenic shock requiring inotropes, and transthoracic echocardiographic (TTE) findings suggestive of BCI. Patients with arrhythmia in the medical history, congestive heart failure, ischemic heart disease, history of cardiac surgery, and those <16years of age were excluded. The BCI rate was 25% in thoracic injuries. The sensitivity and specificity of troponinI, creatine kinase-MB fraction (CK-MB)/creatine kinase (CK) ratio, ECG, and CK-MB/CK ratio plus ECG were 68% and 100%, 50% and 53%, 54.5% and 72%, and 59% and 33%, respectively. Frequency of palpitation, initial CK-MB levels, initial heart rate, frequency of pulmonary contusion, abnormal ECG, and mortality rate were significantly higher in patients with BCI compared with patients without BCI. Pulmonary contusion, accompanying palpitation, Glasgow coma scale (GCS) ≤13, and abnormal ECG findings were important independent parameters increasing the likelihood of BCI on univariate analysis comparing patients with and without BCI. Indicators such as cardiac enzymes and ECG have low sensitivity and specificity when used alone. The reliability of ECG in the diagnosis of BCI decreases in the later hours of trauma.

A reply

Tanqueray and colleagues are correct in stating that a second suction and leucocyte depletion filters are commonly used techniques to diminish the risk of re-infusing fetal and amniotic fluid contaminants and that these were not mentioned in the recent Association of Anaesthetists of Great Britain and Ireland guidelines [1]. Since then an addendum has been sent out mentioning the use of leucocyte depletion filters in obstetrics and published in Anaesthesia News [2]. The use of leucocyte depletion filters to remove possible contaminants during cell salvage was highlighted in the previous paragraph on malignancy, but this was erroneously not repeated in the obstetric section. However, since the excellent review article by Allam et al. [3] was published in January 2008, there have been two developments in the field of cell salvage that are now relevant. Firstly, in August 2008 Sullivan et al. [4] published a small randomised controlled trial showing that amniotic fluid contamination (indicated by alphafetoprotein levels) is not significantly different whether one or two suckers are used, but that more red cells are retrieved with the single suction technique. Although the use of separate suction seems intuitively safer, there is in fact no evidence to support this. This study also confirmed earlier findings [5] that no further reduction in alphafetoprotein is achieved by filtration after washing. The significance of squamous cells in the maternal circulation remains unclear, and while some studies show total removal of these cells by leucocyte depletion filters [6], others suggest that squames persist in up to 7% of those studied but with no discernable clinical effect [4]. It is important to remember that all these clearance studies have been conducted in in-vitro work and whether leucocyte depletion filters make any difference clinically is currently not known. There is good evidence that amniotic fluid routinely enters the maternal circulation at caesarean section with no adverse effect [6]. In addition, before the introduction of the Pall RS Leucocyte Depletion Filter (Pall Medical, Portsmouth UK), several hundred obstetric patients received cell salvaged blood either with no filter or with earlier, less effective filters that have been shown to allow the passage of fetal material, again with no adverse effects [7]. A recent report in Vox Sanguinis described, in a prospective case series of 212 patients with ectopic pregnancies, the effective use of unwashed and unfiltered cell salvaged blood without apparent adverse outcome [8]. In individual maternity units in the United Kingdom, the use of leucocyte depletion filters varies; some units do not use them (personal communication, Dr S Catling; October 2009) and there has been no evidence of amniotic fluid embolus syndrome. In June 2009 the 12th Annual Serious Hazards of Transfusion Report (SHOT) [9] highlighted five cases in which unexpected hypotension occurred as cell-salvaged blood was administered via leucocyte depletion filters; one of these cases is obstetric where severe hypotension was witnessed during re-infusion of salvaged blood through a leucocyte depletion filter. While there is currently no convincing evidence that the leucocyte depletion filter was the cause of these reactions, this is currently under investigation by SHOT and the UK Cell Salvage Action Group. There is a theoretical mechanism by which this could occur, involving the release of vasoactive substances from white blood cells trapped on the negative filter surface [10, 11] This phenomenon was identified by the Food and Drug Administration in 1999 in a Public Health Notification and involved bedside filtration of allogeneic blood. Accordingly, it may be time to justify the routine use of leucocyte depletion filters: the evidence for the compulsory use of leucocyte depletion filters is not compelling, and for the first time there is a possible suggestion of harm. Like the authors, currently we continue to advocate their routine use, but would not hesitate to remove the filter if necessary, particularly when salvaged blood is required to be re-infused under pressure or if there is unexplained hypotension shortly following re-infusion of salvaged blood.

Incidence, Clinical Features and Outcome of Patients with Differentiation Syndrome in Acute Promyelocytic Leukemia Treated with All-Trans Retinoic Acid (ATRA) Alone Versus ATRA Plus Idarubicin Versus ATRA Plus Arsenic Trioxide.

Abstract 1044Poster Board I-66 Background:Differentiation Syndrome (DS) in patients (pts) with acute promyelocytic leukemia (APL) remains a source of significant morbidity and mortality. DS is reported in 2-27% of pts with newly diagnosed APL treated with all-trans retinoic acid (ATRA) alone or in combination with idarubicin (IDA). More recently, arsenic trioxide (ATO) has been used in combination with ATRA as frontline therapy to improve rates of complete remission (CR) and overall survival (OS). It has been postulated that with the use of ATO, the risk of DS may decrease. AimTo describe the incidence, characteristics and outcome of differentiation syndrome with various modalities of ATRA-based therapy used for APL. Methods:We reviewed the records of 167 pts with newly diagnosed APL treated at our institution from 1992-2009 with three regimens: ATRA + IDA (Group 1), liposomal ATRA (Group 2) and ATRA plus ATO (Group 3). Patients in Group 1 (n=52; 1992-1997) received induction with ATRA 45mg/m2 orally daily in two divided doses until CR and IDA 12mg/m2 IV daily for 4 days. Group 2 (n=34; 1997-2000) received liposomal ATRA at 90mg/m2 IV every other day until CR. Patients in Group3 (n=82; 2002-2009) received 45mg/m2 ATRA orally daily in two divided doses, 9mg/m2 gemtuzumab ozogamicin if the WBC count exceeded 30 ×109/L in the first 4 weeks of therapy, ATO 0.15mg/kg/day IV starting on day 10 in 47 patients and on day 1 in 35 patients, and methylprednisolone (50 mg daily for 5 days) to prevent DS. A diagnosis of DS was made by the presence of: dyspnea, unexplained fever, weight gain, peripheral edema, unexplained hypotension, acute renal failure or congestive heart failure, and particularly by a chest radiograph demonstrating interstitial pulmonary infiltrates, or pleuropericardial effusion [Sanz MA, Blood. 2009;113(9):1875-91].Patients with ≥4 features were classified as having severe DS and those with ≤3 mild DS. No single sign or symptom was considered sufficient for diagnosis of DS. Patients with a final diagnosis of pneumonia, sepsis, diffuse alveolar hemorrhage and decompensated heart failure were not considered to have DS. Patients who developed DS ≤7 days of starting therapy with ATRA were classified as “early DS” and others as having “late DS”. Results:Forty one patients (24%) were diagnosed with DS: 14 (27%) in Group 1, 12 (35%) in Group 2, and 15 (18%) in Group 3. Baseline characteristics of patients with DS in each group are shown in Table. Dyspnea, weight gain and pulmonary infiltrates were the most common features of DS in all groups. The median number of days to develop DS after starting ATRA was 3 (1-15) in Group 1, 5 (2-18) in Group 2 and 10 (1-18) in Group 3. ATRA was held in 8 pts (57%) in Group 1, 9 pts (75%) in Group 2, and 8 pts (53%) in Group 3. Intravenous corticosteroids were used for treatment of all patients with DS. CR was achieved in 7 (50%) pts in group 1, 10 (83%) in Group 2 and 14 (93%) in Group 3. The number of patients who died during induction therapy was 6, 2 and 1 in Groups 1, 2 and 3 respectively. There were no deaths directly attributable to DS in any groups. Three-year survival was 65% for pts with DS and 83% for those without DS (p-value: 0.07). Conclusion:The incidence of DS is higher when ATRA alone is used as frontline therapy for APL. With ATRA + ATO (and prophylaxis with corticosteroids) there is a trend for decreased frequency and more delayed occurrence of DS. The severity of DS appears lower for patients not receiving chemotherapy with ATRA. With adequate management, a diagnosis of DS during induction therapy for APL does not influence outcomes independent of therapy.CharacteristicsGroup 1Group 2Group 3TotalDS14/52 (27%)12/34 (35%)15/82 (18%)41/167 (24%)Median age, yrs (range)42 (22-67)37 (10-77)45 (18-74)43 (10-77)Sex (M/F)8/67/58/723/18ECOG*0-16 (43)6 (50)13 (87)25 (61)2-38 (57)6 (50)2 (13)16 (39)WBC (K/μL)< 107 (50)8 (67)9 (60)24 (59)≥ 107 (50)4 (33)6 (40)17 (41)Platelets (K/μL)< 406 (43)9 (75)9 (60)24 (59)≥ 408 (57)3 (25)6 (40)17 (41)SeverityMild7 (50)7 (58)6 (40)20 (49)Severe7 (50)5 (42)9 (60)21 (51)Time course*Early12 (86)8 (67)6 (40)26 (63)Late2 (14)4 (33)9 (60)15 (37)Median time to develop DS*, days3 (1-15)5 (2-18)10 (2-18)4 (1-18)ATRA held8 (57)9 (75)8 (53)25 (61)Dialysis*3 (21)0 (0)1 (7)4 (10)Ventilation*6 (43)1 (8)2 (13)9 (22)*p-value <0.05; otherwise all NS Disclosures:Ravandi:Cephalon: Consultancy, Honoraria.

Unexplained and prolonged perioperative hypotension after orthotopic liver transplantation: Undiagnosed systemic mastocytosis

Arterial vasodilation is common in end-stage liver disease, and systemic hypotension often may develop, despite an increase in cardiac output. During the preparation for and the performance of orthotopic liver transplantation, expected and transient hypotension may be caused by induction agents, anesthetic agents, liver mobilization, or venous clamping. A mild decrease of the already low systemic vascular resistance is often observed, and intermittent use of short-acting agents for vasopressor support is not uncommon. In this report, we describe a patient with unexpected and prolonged hypotension due to vasodilation during and after orthotopic liver transplantation. The preoperative end-stage liver disease evaluation, intraoperative events, and intensive care unit course were reviewed, and no cause for the vasodilation and prolonged hypotension was evident. The explant pathology report was later available and showed systemic mastocytosis. We hypothesize that the unexpected hypotension and vasodilation were caused by mast cell degranulation and its systemic effects on arterial tone.

Unexplained hypotension: The spectrum of dynamic left ventricular outflow tract obstruction in critical care settings*

To illustrate the clinical and hemodynamic abnormalities caused by dynamic left ventricular outflow tract obstruction (LVOTO) in critical care setting. We reviewed cases referred to Cardiology with echocardiographic evidence of LVOTO and their clinical presentations. We present those cases where LVOTO can transiently occur without hypertrophic cardiomyopathy when inotropic agents are used for hypotension. Five women in the 50-70 age range and prior history of hypertension presented with various symptoms like chest discomfort, fatigue, dizziness, atrial fibrillation, and hypotension. An ejection systolic murmur was noted most often in the left third intercostal space and ECG revealed ST-T wave abnormalities. LVOTO caused by mitral systolic anterior motion was detected by echocardiography and catheterization excluded acute coronary disease. In critical care setting, LVOTO can occur due to apical ballooning syndrome, coronary disease, medications, volume depletion, and valvular abnormalities. Because this condition mimics acute coronary syndrome or other etiologies of hypotension in medical and surgical intensive care units, appropriate treatment can be delayed. Nonhypertrophic cardiomyopathy LVOTO usually responds well to fluid replacement, beta blockers, and medication changes. LVOTO should be suspected especially in women presenting with hypotension and systolic murmur in critical care settings. Clinical acumen and timely echocardiography are required to effectively counter this transient but potentially lethal problem.

Requirement of Perioperative Stress Doses of Corticosteroids

To determine the requirement for perioperative supplemental (stress) doses of corticosteroids in patients receiving long-term corticosteroid therapy and undergoing a surgical procedure. Corticosteroids are among the most commonly prescribed medications and will predictably result in suppression of the hypothalamic-pituitary-adrenal axis with long-term use. Patients receiving therapeutic dosages of corticosteroids frequently require surgery; these patients are almost universally treated with stress doses of corticosteroids during the perioperative period. MEDLINE, EMBASE, Cochrane Register of Controlled Trials, and citation review of relevant primary and review articles. Randomized controlled trials (RCTs) comparing stress doses of corticosteroids with placebo and cohort studies that followed up patients after surgery in which perioperative stress doses of corticosteroids were not administered. Data were abstracted on the study design, study size, study setting, patient population, dosage and duration of previous corticosteroid therapy, adrenal function testing results, surgical intervention, corticosteroid dosing regimen, intraoperative and postoperative hemodynamic profile, and incidence of adrenal crisis. Nine studies met our inclusion criteria, including 2 RCTs and 7 cohort studies. These studies enrolled a total of 315 patients who underwent 389 surgical procedures. In the 2 RCTs, there was no difference in the hemodynamic profile between patients receiving stress doses of corticosteroids compared with patients receiving only their usual daily dose of corticosteroid. In the 5 cohort studies in which patients continued to receive their usual daily dose of corticosteroid without the addition of stress doses, no patient developed unexplained hypotension or adrenal crisis. One patient in each of the 2 cohort studies (5% and 1% of the cohort) in which the usual daily dose of corticosteroid was stopped 48 and 36 hours before surgery developed unexplained hypotension; both of these patients responded to hydrocortisone and fluid administration. Patients receiving therapeutic doses of corticosteroids who undergo a surgical procedure do not routinely require stress doses of corticosteroids so long as they continue to receive their usual daily dose of corticosteroid. Adrenal function testing is not required in these patients because the test is overly sensitive and does not predict which patient will develop an adrenal crisis. Patients receiving physiologic replacement doses of corticosteroids owing to primary disease of the hypothalamic-pituitary-adrenal axis, however, require supplemental doses of corticosteroids in the perioperative period.

Systolic anterior motion of the mitral valve leaflet leading to haemodynamic compromise

We report a case of systolic anterior motion of the mitral valve leaflet during a coronary artery bypass graft surgery causing ST-T changes and hypotension. Anaesthetic induction and cardiopulmonary bypass were uncomplicated with minimal inotropic support. The elderly patient received 1000 ml of colloid and 700 ml of pump blood. While the heart rate was 80 min−1 with a mean arterial pressure of 70 mmHg, ST segment changes were noted with the surgical closure of chest. More colloids were infused and the systolic blood pressure remained around 90–100 mmHg. The chest was reopened, the heart continued to contract well, the surgeon was confident of the integrity of the grafts but the ST segment progressed to −2.0 mm. Dopamine was increased to 10 μg.kg.min−1 and the ST dipped to −3.5 mm. At this point, the blood pressure started dropping and the heart rate increased to 100 min−1. An intra-aortic balloon was inserted, noradrenaline was started; subsequently transoesophageal echocardiography was performed. The left ventricle was empty and contracting vigorously without any wall motion changes. Significant anterior motion of the mitral valve leaflet during systole was observed causing obstruction of the outflow tract (2, 3). More fluids were infused and inotropic support was stopped. The ST depression reverted back to normal, with good control of heart rate and blood pressure. Transoesophageal echo showing systolic anterior motion. Diagrammatic representation of long axis transoesophageal echo in Fig. 2 showing systolic anterior motion. Systolic anterior motion is an important feature of idiopathic hypertrophic subaortic stenosis [1]. It can be an associated finding in patients without any organic heart disease [2] and can be fatally symptomatic in extreme hypovolaemia [3]. Systolic anterior motion appears to be a non-specific motion of mitral valve leaflets occurring in vigorously contracting volume depleted, completely obliterated systolic cavities. Death from systolic anterior motion has been reported in severely ill patients without pre-existing cardiac disease [3]. The extent of hypovolaemia caused by vasodilatation from most anaesthetic drugs and regional anaesthesia is often underestimated, leading to inadequate fluid replacement and inappropriate infusion of inotropes. Judicious infusion of fluids did not improve the situation in our case, probably because the vasodilatation of general anaesthesia and cardiopulmonary bypass were underestimated. Echocardiography allowed visualisation of the anterior motion of the leaflets, hypercontractile ventricles and acute mitral regurgitation. Although transoesophageal echocardiography is superior to transthoracic echo-cardiography [4], in unexplained hypotension, transthoracic echo-cardiography could be used if the anterior chest wall can be exposed [5]. Though rare, severe systolic anterior motion in acute hypotensive episodes can go unrecognised causing severe cardiovascular compromise. The treatment of severe systolic anterior motion should be mainly fluids, vasopressor drugs and control of tachycardia. Echocardiography is useful not only in diagnosing systolic anterior motion, but to visualise empty hyperdynamic ventricles and in preventing further complications.

The importance of genus Candida in human samples

Microbiology is a rapidly changing field. As new researches and experiences broaden our knowledge, changes in the approach to diagnosis and therapy have become necessary and appropriate. Recommended dosage of drugs, method and duration of administration, as well as contraindications to use, evolve over time all drugs. Over the last 2 decades, Candida species have emerged as causes of substantial morbidity and mortality in hospitalized individuals. Isolation of Candida from blood or other sterile sites, excluding the urinary tract, defines invasive candidiasis. Candida species are currently the fourth most common cause of bloodstream infections (that is, candidemia) in U.S. hospitals and occur primarily in the intensive care unit (ICU), where candidemia is recognized in up to 1% of patients and where deep-seated Candida infections are recognized in an additional 1 to 2% of patients. Despite the introduction of newer anti-Candida agents, invasive candidiasis continues to have an attributable mortality rate of 40 to 49%; excess ICU and hospital stays of 12.7 days and 15.5 days, respectively, and increased care costs. Postmortem studies suggest that death rates related to invasive candidiasis might, in fact, be higher than those described because of undiagnosed and therefore untreated infection. The diagnosis of invasive candidiasis remains challenging for both clinicians and microbiologists. Reasons for missed diagnoses include nonspecific risk factors and clinical manifestations, low sensitivity of microbiological culture techniques, and unavailability of deep tissue cultures because of risks associated with the invasive procedures used to obtain them. Thus, a substantial proportion of invasive candidiasis in patients in the ICU is assumed to be undiagnosed and untreated. Yet even when invasive candidiasis is diagnosed, culture diagnosis delays treatment for 2 to 3 days, which contributes to mortality. Interventions that do not rely on a specific diagnosis and are implemented early in the course of Candida infection (that is, empirical therapy) or before Candida infection occurs (that is, prophylaxis) might improve patient survival and may be warranted. Selective and nonselective administration of anti-Candida prophylaxis is practiced in some ICUs. Several trials have tested this, but results were limited by low statistical power and choice of outcomes. Thus, the role of anti-Candida prophylaxis for patients in the ICU remains controversial. Initiating anti-Candida therapy for patients in the ICU who have suspected infection but have not responded to antibacterial therapy (empirical therapy) is practiced in some hospitals. This practice, however, remains a subject of considerable debate. These patients are perceived to be at higher risk from invasive candidiasis and therefore are likely to benefit from empirical therapy. Nonetheless, empirical anti-Candida therapies have not been evaluated in a randomized trial and would share shortcomings that are similar to those described for prophylactic strategies. Current treatment guidelines by the Infectious Diseases Society of America (IDSA) do not specify whether empirical anti-Candida therapy should be provided to immunocompetent patients. If such therapy is given, IDSA recommends that its use should be limited to patients with Candida colonization in multiple sites, patients with several other risk factors, and patients with no uncorrected causes of fever. Without data from clinical trials, determining an optimal anti-Candida strategy for patients in the ICU is challenging. Identifying such a strategy can help guide clinicians in choosing adequate therapy and may improve patient outcomes. In our study, we developed a decision analytic model to evaluate the cost-effectiveness of empirical anti-Candida therapy given to high-risk patients in the ICU, defined as those with altered temperature (fever or hypothermia) or unexplained hypotension despite 3 days of antibacterial therapy in the ICU.

Innovations in PAD therapy

Innovations in PAD therapy

The complications of percutaneous endoscopic gastrostomy

Percutaneous endoscopic gastrostomy (PEG) has become the primary procedure for the long-term nutrition of patients with swallowing disorders. It has been shown to be an effective method with a lower complication rate than surgical placement [1]. It can be performed in the intensive care unit, but complications may occasionally occur. The estimated incidence of major complications is 8% [2]. Abscess and wound infections are the most frequent complications, but necrotizing fasciitis, colon or small bowel injuries, gastrocolic fistula, duodenal hematoma, liver injury, gastric perforation, and catheter migration have also been described [3]. Unexpectedly, acute hemorrhage following PEG is rarely reported. In the literature, we found only one case report of a fatal retroperitoneal hemorrhage occurring 2 hours after a PEG [4]. In a series of 263 cases, Schurink and colleagues [2] described only two cases of intra-abdominal bleeding. A 59-year-old man was admitted to our hospital with intracerebral hemorrhage. On day 40, a PEG was performed in the intensive care unit using the 'pull' technique as previously described [5]. The needle puncture of the stomach was accomplished only on the second attempt, although the rest of the procedure was completed uneventfully. The material used was the Bard®Fastrac™ Pull PEG Kit (Bard Access Systems, Salt Lake City, USA). One hour after the end of the procedure, the patient presented a tachycardia (120 beats per minute), with cardiovascular collapse (arterial pressure 70/50 mmHg). Physical examination revealed a distended abdomen. The hemoglobin concentration was 5.5 g/dL. Abdominal echography showed the presence of intraperitonal liquid. An emergency laparotomy was performed, revealing a massive hemoperitoneum due to active bleeding from a small vessel of the minor curvature. X-sutures were applied and the bleeding stopped. A gastrostomy was recreated at the end of surgery. The massive hemoperitoneum we described is a rare complication in relation to its rapidity and its severity. We think that the initial, unsuccessful passage of the needle could have caused the gastric artery branch laceration. Indeed, such a mechanism of injuries has already been suggested as an explanation for a fatal retroperitoneum due to breaches in the splenic and superior mesenteric veins [4]. In the patient we described, prompt recognition could minimize morbidity. Although generally considered safe, PEG can be associated with life-threatening bleeding, especially when multiple needle punctures have been made. It presents with unexplained postprocedure hypotension. Intensivists who are used to performing PEG should be aware of this complication because early recognition and treatment are essential.

Acute myocarditis after massive phenelzine overdose

Monoamine oxidase inhibitors (MAOIs) are uncommonly used due to their high frequency of adverse effects, including tachycardia and hypertension. Recently, there has been renewed interest in the role of this class of drugs in treating a variety of psychiatric disorders. The clinical features of MAOI overdose are poorly characterised. This paper describes a novel cardiac complication of phenelzine toxicity in a previously healthy young adult with no history of cardiovascular disease. A 23-year-old woman presented to hospital after massive phenelzine overdose, and the clinical features and pathological findings are discussed in light of existing literature. Clinical features of phenelzine toxicity included reduced consciousness level, seizures, and tachycardia, in keeping with previous reports. Unexpectedly, the patient developed severe and unexplained hypotension and impaired left ventricular function, and died 3 days after initial presentation. Post-mortem examination confirmed high serum phenelzine concentrations (4.1 mg/L) and histopathological features that were consistent with drug-induced acute myocarditis. Acute myocarditis was attributed to phenelzine in the absence of any plausible alternative explanation. This possible complication should be considered in patients who develop unexplained hypotension after phenelzine overdose.

Importance of bedside echocardiography for detection of unsuspected isolated right ventricular infarction as a cause of cardiovascular collapse

Isolated right ventricular infarction is a rare and commonly overlooked condition, because of scarce electrocardiographic changes. We present 2 cases of isolated right ventricular infarction that went unrecognized in the ED. Both patients presented with signs of circulatory collapse, third-degree atrioventricular block, and without prominent ischemic changes in the electrocardiogram. Diagnosis was further obfuscated by the absence of chest pain and atypical clinical presentation with left-hand paresis in one patient and hypothermia in the second. Echocardiography was performed as part of the evaluation of unexplained hypotension. In both cases, it revealed right ventricular dysfunction, which suggested possible acute right ventricular infarction. Diagnosis was confirmed by the finding of subtotal ostial thrombotic occlusions of the right coronary artery in both cases. Echocardiography played a decisive role in the diagnostic procedure, enabling prompt therapeutic intervention and subsequent resolution of shock.

Hospital Mortality Due to Pulmonary Embolism (PE) and an Evaluation of the Usefulness of Preventative Interventions.

Background: Many hospitalized patients with PE die. A large registry study described a mortality rate of 17.4% in patients with PE and suggested 45% of these deaths were due to the PE. Data on death and PE is usually derived retrospectively from hospital databases without chart confirmation and to our knowledge no study has attempted to determine the accuracy of coding for PE deaths. Furthermore, it is unclear how often deaths caused by PE could have been prevented.Methods: A retrospective chart review of PE cases hospitalized at a tertiary care center. Charts over an 8 year period ending in 2004 were reviewed if the hospital database record identified PE as a diagnosis by the ICD-10 coding system. Charts of those who died were independently reviewed by two thrombosis experts with discrepancies resolved by consensus or a third reviewer. Prior to chart review definitions were agreed upon. The coding as PE was considered correct (confirmed PE) if there was supportive imaging, an autopsy, or in the case of death without imaging or autopsy, the clinical scenario was such that PE could have occurred. The degree of certainty that PE contributed to the death was classified as certain (unexplained hypotension, hypoxia, cardiac arrest with no other explanation other than PE and autopsy confirmation or radiographic confirmation), highly probable (same as certain but no autopsy confirmation), probable (criteria for highly probable but another disease could have caused the death). We considered these cases to be death due to PE. Deaths were also classified as possible (other cause suspected based on clinical evidence but 100% certainty not available), or unlikely due to PE (all other cases). In cases defined as death due to PE we determined whether any further intervention could have prevented death.Results: 612 cases were identified of whom 68 had radiographic or autopsy data that ruled out the diagnosis and in 46 the coding was clearly an error. 498 cases of PE were identified, 111 of whom died during hospitalization; the mortality rate in those the hospital coded as PE was 18% vs 22% of those with confirmed PE. Death due to PE was diagnosed in 70 patients (14% of patients with confirmed PE and 11% of all patients coded as PE). In the remaining 41 deaths, PE was possible in 24 and unlikely in 17. Disagreement was uncommon. There was no difference between the likelihood of death from PE in the group diagnosed by imaging and autopsy compared with the group where PE death was confirmed by an appropriate clinical scenario. 38 deaths due to PE may have been prevented with an additional intervention: prophylaxis (55%), earlier diagnosis (45%), inferior vena cava filter (IVCF) (32%), anticoagulation (18%), embolectomy 5%, thrombolytics (3%). The remaining deaths due to PE were not preventable since 15 patients were palliative and did not receive active treatment, 9 died before a diagnosis was made and in 8 another disease prevented treatment.Conclusions: Using hospital database records is a reasonable means to evaluate PE mortality and our death due to PE rates are similar to those in registry publications. Surprisingly imaging and autopsy results do not increase the probability of reaching the conclusion that death is due to PE. Over half of preventable PE deaths may have been prevented by prophylaxis and one third with an IVCF.

Indolent Systemic Mastocytosis as the Cause of a Long History of Unexplained Hypotensive Episodes

Assessment of patients with unexplained hypotensive episodes in outpatient practice is often challenging, with an extensive differential diagnosis. The prevalence of systemic mast cell disease (MCD) is unknown, and the diagnosis is often elusive because serum and urine markers may become positive only after one of the self-limited, recurrent hypotensive episodes. Nevertheless, MCD is increasingly recognized as a cause of unexplained hypotension, secondary osteoporosis, and anaphylactic reactions to Hymenoptera stings. We describe a 38-year-old man who had a 15-year history of undiagnosed, recurrent hypotensive episodes with stereotypic symptoms. Extensive evaluation during these years was unrevealing. On physical examination, he appeared to be a healthy man with a prominent macular rash. Results of skin biopsy showed tryptase-positive mast cells. He had markedly elevated serum tryptase levels, and results of bone marrow biopsy revealed 10% mast cells; all these findings were consistent with indolent systemic mastocytosis. Key features in his history and physical examination prompted the conclusive testing. The most telling features were hypotension, tachycardia, and the rash (urticaria pigmentosa).

Pericardial Fat Mimicking Pericardial Effusion on Two‐Dimensional Echocardiography

A 78-year-old overweight woman with diabetes mellitus, bronchial asthma, and Sheehan's syndrome on chronic steroid therapy presented with mild short-lived hematemesis, significant hypotension disproportionate to the degree of bleeding and radiographic evidence of cardiomegaly. Endoscopy showed duodenal ulcer. During evaluation of the unexplained brief hypotension and cardiomegaly, 2D-echocardiogram demonstrated anterior and posterior echo-free spaces consistent with large pericardial effusion (PE). However, subsequent elective surgical pericardiotomy unexpectedly revealed large amounts of pericardial fat. Pericardial fat was also noted on magnetic resonance imaging of the chest. Our case illustrates a potential pitfall of 2D-echocardiography in the diagnosis of PE.

Relative Adrenal Insufficiency Among Trauma Patients in a Community Hospital

The integrity of the hypothalamic-pituitary-adrenal (HPA) axis is a major determinant of the host response to stress. Recent studies have proven that low doses of hydrocortisone and fludrocortisone can significantly reduce mortality in patients with relative adrenal insufficiency (RAI) without increasing adverse events. This study was a retrospective chart review of patients in a community hospital who carried the diagnosis of both adrenal insufficiency and trauma. Over a 16-month period, the incidence of RAI among severely injured patients (injury severity score >/= 13) was 3%. Only 1 patient had the classic electrolyte findings of adrenal insufficiency, but all had vasopressor-dependent hypotension. Our patients had an average intensive care unit day stay of 37 days and were not tested for RAI on average until day 20 of their intensive care unit stay. Random cortisol levels did not correlate with injury severity. Six patients (75%) had a positive hemodynamic response to steroids. Relative adrenal insufficiency after trauma is rare. In RAI, clear signs and symptoms are usually absent. The clinical diagnostic clue may be the unexplained hypotension and the resistance to inappropriately high doses of inotropes and vasoactive agents. The hemodynamic profile often shows a hyperdynamic state of high cardiac output and a low systemic vascular resistance. Baseline serum cortisol levels did not correlate with injury severity scores in this group of patients, which suggests a defect in the HPA axis. An intensive care unit day stay of greater than or equal to 20 days, ventilator dependence/acute respiratory distress syndrome, and a hyperdynamic state mandates consideration of endocrine testing to exclude RAI. Physiologic doses of hydrocortisone can reverse this potentially life-threatening syndrome.