[Show abstract][Hide abstract] ABSTRACT: Background Miosis occurs following exposure to toxins that decrease the sympathomimetic tone, increase the cholinergic tone, or exert sedative-hypnotic effects, but has not been reported in insulin poisoning. Case Report A 64-year- old woman without co-morbidities was found unconscious next to an empty insulin pen. Her Glasgow Coma Scale was 3 with absent reflexes, bilateral reactive miosis, and injection marks across the abdominal wall. The patient was endotracheally intubated, mechanically ventilated, and transferred to this hospital. At admission, the blood glucose level was 34 mg/dL. Glasgow Coma Scale remained at 3, with persistent bilateral reactive miosis. The toxicology screening was negative for ethanol, barbiturates, tricyclic antidepressants, phenothiazines, amphetamines, cannabinoids, salicylates, acetaminophen, and cocaine. Cranial computed tomography with angiography and magnetic resonance imaging (MRI) did not show any structural brain lesions. Intravenous glucose was continued at 6-14 g/h for 3 days. On repeated neurological examinations, the patient remained deeply comatose, with partial loss of cranial nerve function. Bilateral reactive miosis persisted for 4 days. From day 5 on, the patient awoke progressively. At discharge, the patient was fully alert and orientated, without a focal neurological deficit. Conclusions Prolonged bilateral reactive miosis can be a clinical symptom accompanying metabolic encephalopathy in severe insulin poisoning. Functional impairment of the pons due to relative hypoperfusion during hypoglycemia may serve as a reasonable pathophysiologic explanation for this phenomenon.
The American journal of case reports. 01/2015; 16:1-3.
[Show abstract][Hide abstract] ABSTRACT: IntroductionLiberal and over-aggressive use of vasopressors during the initial period of shock resuscitation may compromise organ perfusion and worsen outcome. When transiently applying the concept of permissive hypotension it would be helpful to know at which arterial blood pressure terminal cardiovascular collapse occurs.Methods
In this retrospective cohort study, we aimed to identify the arterial blood pressure associated with terminal cardiovascular collapse in 140 patients who died in the intensive care unit while being invasively monitored. Demographic data, co-morbid conditions and clinical data at admission, during 24 hours before and at the time of terminal cardiovascular collapse were collected. The systolic, mean and diastolic arterial blood pressure immediately before terminal cardiovascular collapse was documented. Terminal cardiovascular collapse was defined as an abrupt (<5 min) and exponential decrease in heart rate (>50% compared to preceding values) followed by cardiac arrest.ResultsThe mean¿±¿standard deviation (SD) of the systolic, mean and diastolic arterial blood pressure associated with terminal cardiovascular collapse was 47¿±¿12, 35¿±¿11 and 29¿±¿9 mmHg. Patients with congestive heart failure (39¿±¿13 versus 34¿±¿10 mmHg; P¿=¿0.04), left main stem stenosis (39¿±¿11 versus 34¿±¿11 mmHg; P¿=¿0.03) or acute right heart failure (39¿±¿13 versus 34¿±¿10 mmHg; P¿=¿0.03) had higher arterial blood pressures than patients without these risk factors. Patients with severe valvular aortic stenosis had the highest arterial blood pressures associated with terminal cardiovascular collapse (systolic, 60¿±¿20; mean, 46¿±¿12; diastolic, 36¿±¿10 mmHg), but this difference was not significant. Sepsis patients and patients exposed to sedatives or opioids during the terminal phase exhibited lower arterial blood pressures than patients without sepsis or administration of such drugs.Conclusions
The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients was very low and varied with individual co-morbid conditions (for example congestive heart failure, left main stem stenosis, severe valvular aortic stenosis, acute right heart failure), drug exposition (for example sedatives or opioids) and the type of acute illness (for example sepsis).
Critical care (London, England) 12/2014; 18(6):719. · 5.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Hemodialysis is considered the renal replacement technique of choice to control life-threatening hypercalcemia. In this case series, the experience with continuous veno-venous hemodiafiltration (CVVHDF) with regional citrate anticoagulation to control five hypercalcemic crises in four patients is summarized. Overall maximum ionized and total calcium levels were ranged from 1.72-2.01 mmol/L and 3.1-4.2 mmol/L, respectively. All patients presented with impaired consciousness, cardiac arrhythmias and/or acute oliguria despite therapy. Trisodium-citrate was administered at 3 mmol/h (hourly calcium replacement 1.15-2.75 mmol). This allowed a controlled decrease of ionized calcium levels below 1.4 mmol/L within 4 hours (IQR, 2.5-10) and resolution of neurological symptoms within 15.5 hours (IQR, 12-22.8). The duration of CVVHDF was one day in those patients in whom hypercalcemia was the reason for admission. Four asymptomatic episodes of mild hypocalcemia occurred in two patients. No patient developed relevant abnormalities of serum sodium levels or pH, experienced cardiac arrhythmia or required transfusion of blood products during CVVHDF. One patient with metastatic bronchial carcinoma experienced rebound hypercalcemic crisis thirteen days following a one day session of CVVHDF with regional citrate anticoagulation.In conclusion, CVVHDF with regional citrate anticoagulation appears to be effective and potentially safe to rapidly normalize calcium levels in hypercalcemic crisis.
ASAIO journal (American Society for Artificial Internal Organs: 1992) 12/2014; · 1.39 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Perioperative fluid management plays a fundamental role in maintaining organ perfusion, and is considered to affect morbidity and mortality. Targets according to which fluid therapy should be administered are poorly defined. This systematic review aimed to identify specific targets for perioperative fluid therapy.
[Show abstract][Hide abstract] ABSTRACT: Restoration of adequate tissue perfusion is the goal of resuscitation in septic shock. A growing understanding of microcirculatory dysfunction in sepsis led to a change in resuscitation practice away from targeting arterial and central venous pressures and towards tissue perfusion-guided protocols. This change in the approach to resuscitation was accompanied by a change in the role of vasoconstrictors. This review summarizes the pathophysiological and therapeutic mainstays of septic shock resuscitation and attempts to critically evaluate the scientific evidence on the use of vasopressin as a non-adrenergic vasoconstrictor in septic shock. Based on the published study results vasopressin appears to be of potential benefit in adult patients with moderate septic shock (norepinephrine requirements < 15 μg/min) and lacking signs of systemic hypoperfusion (e.g. normal arterial lactate levels). A vasopressin infusion with the sole target to increase arterial blood pressure despite the presence of systemic hypoperfusion is dangerous and can result in a critical deterioration of tissue perfusion.
[Show abstract][Hide abstract] ABSTRACT: Dermatomyositis is a chronic inflammatory disorder characterized by muscular and dermatologic symptoms with variable internal organ involvement. This is the first report on a patient with acute dermatomyositis and fulminant systemic capillary leak syndrome.
A 69-year-old Caucasian woman with chronic dermatomyositis presented with clinical signs of severe hypovolemic shock and pronounced hemoconcentration (hematocrit, 69%). Her colloid osmotic pressure was 4.6mmHg. Following a bolus dose of prednisolone (500mg), fluid resuscitation was initiated. During volume loading, anasarca and acute respiratory distress rapidly developed. Echocardiography revealed an underfilled, hypokinetic, diastolic dysfunctional left ventricle with pericardial effusion but no signs of tamponade. Despite continued fluid resuscitation and high-dosed catecholamine therapy, the patient died from refractory shock 12 hours after intensive care unit admission. A laboratory analysis of her complement system suggested the presence of C1 inhibitor deficiency as the cause for systemic capillary leakage. The post-mortem examination revealed bilateral pleural, pericardial and peritoneal effusions as well as left ventricular hypertrophy with patchy myocardial fibrosis. Different patterns of endomysial/perimysial lymphocytic infiltrations adjacent to degenerated cardiomyocytes in her myocardium and necrotic muscle fibers in her right psoas major muscle were found in the histological examination.
This case report indicates that acute exacerbation of chronic dermatomyositis can result in a fulminant systemic capillary leak syndrome with intense hemoconcentration, hypovolemic shock and acute heart failure. In the presented patient, the cause for diffuse capillary leakage was most probably acquired angioedema, a condition that has been associated with both lymphoproliferative and autoimmunologic disorders.
[Show abstract][Hide abstract] ABSTRACT: Ventricular torsion is an important component of cardiac function. The effect of septic shock on left ventricular torsion is not known. Because torsion is influenced by changes in preload, we compared the effect of fluid loading on left ventricular torsion in septic shock with the response in matched healthy control subjects.
We assessed left ventricular torsion parameters using transthoracic echocardiography in 11 patients during early septic shock and in 11 age- and sex-matched healthy volunteers before and after rapid volume loading with 250 mL of a Ringer's lactate solution.
Peak torsion and peak apical rotation were reduced in septic shock (10.2 ± 5.2° and 5.6 ± 5.4°) compared with healthy volunteers (16.3 ± 4.5° and 9.6 ± 1.5°; P = 0.009 and P = 0.006 respectively). Basal rotation was delayed and diastolic untwisting velocity reached its maximum later during diastole in septic shock patients than in healthy volunteers (104 ± 16% vs 111 ± 14% and 13 ± 5% vs 21 ± 10%; P = 0.03 and P = 0.034, respectively). Fluid challenge increased peak torsion in both groups (septic shock, 10.2 ± 5.3° vs 12.6 ± 3.9°; healthy volunteers, 16.3 ± 4.5° vs 18.1 ± 6°; P = 0.01). Fluid challenge increased left ventricular stroke volume in septic shock patients (P = 0.003).
Compared with healthy volunteers, left ventricular torsion is impaired in septic shock patients. Fluid loading attenuates torsion abnormalities in parallel with increasing stroke volume. Reduced torsional motion might constitute a relevant component of septic cardiomyopathy, a notion that merits further testing in larger populations.
The Canadian journal of cardiology 12/2013; 29(12):1665-1671. · 3.12 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Definitions of shock and resuscitation endpoints traditionally focus on blood pressures and cardiac output. This carries a high risk of overemphasizing systemic hemodynamics at the cost of tissue perfusion. In line with novel shock definitions and evidence of the lack of a correlation between macro- and microcirculation in shock, we recommend that macrocirculatory resuscitation endpoints, particularly arterial and central venous pressure as well as cardiac output, be reconsidered. In this viewpoint article, we propose a three-step approach of resuscitation endpoints in shock of all origins. This approach targets only a minimum individual and context-sensitive mean arterial blood pressure (for example, 45 to 50 mm Hg) to preserve heart and brain perfusion. Further resuscitation is exclusively guided by endpoints of tissue perfusion irrespectively of the presence of arterial hypotension ('permissive hypotension'). Finally, optimization of individual tissue (for example, renal) perfusion is targeted. Prospective clinical studies are necessary to confirm the postulated benefits of targeting these resuscitation endpoints.
Critical care (London, England) 10/2013; 17(5):326. · 5.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: One of the rationales for the use of vasopressin in septic shock has been its potential cardioprotective mechanisms. Lower heart rates, higher arterial pressures, and fewer norepinephrine doses during vasopressin therapy were hypothesized to protect the heart from myocardial ischemia. In a prospective sub-study of the VASST (Vasopressin in Septic Shock Trial) project, Mehta and colleagues specifically evaluated this hypothesis but failed to find lower cardiac biomarkers or fewer ischemic electrocardiogram changes in patients receiving vasopressin compared with subjects receiving norepinephrine alone. After recent evidence of a lacking survival benefit, the present study results further challenge the future role of vasopressin as a vasopressor in septic shock.
Critical care (London, England) 10/2013; 17(5):1002. · 5.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: In this prospective, observational study, the rate of antibiotic resistance in cultures sampled from sepsis patients was determined in an intensive care unit of a low-middle income country.
Critically ill patients suffering from bacterial sepsis were eligible for enrollment. Aside from demographic, disease-related and sepsis-specific parameters, the type of microbiological sample and cultured microorganism as well as the resistance pattern (extensively resistant bacteria, multi-drug resistant bacteria) were documented. Descriptive statistical methods, parametric and non-parametric tests were used.
215 sepsis patients were included. 193 ofthe 410 cultured organisms (47.1%) showed antibiotic resistance [extensively resistant bacteria, n = 90 (11%); multi-drug resistant bacteria, n = 103 (25.1%)]. 51.6% of the patients were infected by > or = 1 resistant bacteria. Bacteria with an exceptionally high rate of antibiotic resistance were Acinetobacter baumannii (90%), Enterobacter spp (60%) and coagulase-negative Staphylococci (60%). Patients infected with resistant bacteria more often received inadequate empirical antibiotic therapy (36.9 vs. 13.5%, p < 0.001), required mechanical ventilation (66.7 vs. 42.3%, p < 0.001) and renal replacement therapy (28.8 vs. 9.6%, p < 0.001) more frequently, and had a longer stay in the intensive care unit [5 (3-9.5) vs. 5 (2-8)%, p < 0.001] than patients with sepsis due to non-resistant bacteria. There was a trend towards a higher mortality in patients with resistant bacteria (43.2 vs. 31.7%, p = 0.09).
Resistant bacteria were detected in up to 50% of microbiological samples from critically ill sepsis patients in the intensive care unit of a low-middle-income country. Antibiotic resistance appears to be a relevant problem of sepsis management in a resource-limited setting.
Middle East journal of anaesthesiology 10/2013; 22(3):293-300.
[Show abstract][Hide abstract] ABSTRACT: PURPOSE: A heart rate >90 bpm serves as one of four characteristics defining the systemic inflammatory response syndrome and is used in scoring systems to predict in-hospital mortality of intensive care unit (ICU) patients. Despite its central role in critical illness, specific data regarding the relationship between heart rate and outcome are rare. METHODS: In this post hoc analysis of a prospectively collected database, we analyzed the value of heart rate averaged from four predefined time points during the last 24 h before ICU discharge as a predictor of post-ICU in-hospital and post-hospital mortality in medical ICU patients. Furthermore, the relationship between heart rate and inflammation, as well as the influence of rate control medications on the association between heart rate and outcome were identified. RESULTS: Among the 702 ICU patients discharged from the ICU, 7.1 % died before hospital discharge. At 4 years of follow-up, post-hospital mortality was 14.4 %. Multivariate Cox proportional hazards models revealed heart rate before ICU discharge (HR 5.95; 95 % CI 1.24-28.63; p = 0.03) as an independent predictor of post-ICU in-hospital mortality. Both heart rate (HR 2.56; 95 % CI, 1.05-6.34; p = 0.04) and the C-reactive protein serum concentration before ICU discharge (HR, 1.26; 95 % CI, 1.09-1.46; p = 0.002) were independently associated with post-hospital mortality. Heart rate control therapy reduced the risk of post-ICU in-hospital (HR 0.38; 95 % CI, 0.18-0.81; p = 0.01) and post-hospital (HR, 0.47; 95 % CI, 0.22-1.00; p = 0.05) mortality. CONCLUSION: Heart rate evaluated 24 h before ICU discharge was independently associated with post-ICU in-hospital and post-hospital mortality. Pharmacological interventions to control heart rate may beneficially influence post-ICU mortality.
Clinical Research in Cardiology 04/2013; · 4.17 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Myocardial depression in septic shock is well-known but its pathophysiological genesis is incompletely understood. To assess the incidence and extent of stress-induced histologic myocardial alterations in septic shock a prospective, observational, clinical and post-mortem study was conducted and twenty patients dying from septic shock were included. Exclusion criteria were <18 years, pregnancy, open heart surgery or cardiopulmonary resuscitation, acute neurologic diseases, pheochromocytoma, and forensic autopsy. A systematic macropathologic evaluation was performed. Nine predefined heart sections were histologically screened for myocytolysis, interstitial fibrosis, contraction band necrosis, mononuclear infiltrates, interstitial edema, and tissue hemorrhage. Stress-induced pathologies were found in 90-100% of patients in all heart sections (myocytolysis, 100%; interstitial fibrosis, 100%; contraction band necrosis, 95%; mononuclear infiltrates, 90%; interstitial edema, 90%; tissue hemorrhage, 30%). The incidence and extent of contraction band necrosis, mononuclear infiltrates, and myocytolysis did not differ between genders, patients with or without chronic ß-blocker, calcium-antagonist and/or statin premedication, or between the binary use of different catecholamine agents (all comparisons p>0.05). The maximum epinephrine dose correlated with the overall extent of mononuclear infiltrates (Spearman-Rho, r=0.704; p=0.05) and myocytolysis (Spearman-Rho, r=0.933; p=0.001). Maximum norepinephrine doses correlated with the extent of mononuclear infiltrates in the left ventricular anterior wall (Spearman-Rho, r=0.519; p=0.02). The total duration of catecholamine therapy was correlated with the extent of mononuclear infiltrates in the apex (Spearman-Rho, r=0.571; p=0.009) and right atrium (Spearman-Rho, r=0.535; p=0.02). In conclusion, our results suggest that histologic lesions potentially indicative of stress-induced cardiotoxicity can be observed in the majority of patients succumbing to septic shock.
[Show abstract][Hide abstract] ABSTRACT: Introduction
La torsion ventriculaire est une composante importante du fonctionnement cardiaque. On ne connaît pas l'effet du choc septique sur la torsion du ventricule gauche. Puisque les modifications en précharge influencent la torsion, nous avons comparé l'effet du remplissage sur la torsion du ventricule gauche lors de choc septique chez les témoins appariés en santé.
Nous avons évalué les paramètres de la torsion du ventricule gauche à l'aide de l'échocardiographie transthoracique chez 11 patients durant la phase précoce du choc septique et chez 11 volontaires en santé appariés selon l'âge et le sexe avant et après la charge volumique rapide de 250 ml d'une solution de Ringer lactate.
La torsion maximale et la rotation apicale maximale ont été réduites lors d'un choc septique (10,2 ± 5,2 et 5,6 ± 5,4) comparativement aux volontaires en santé (16,3 ± 4,5 et 9,6 ± 1,5; P = 0,009 et P = 0,006, respectivement). La rotation basale a été retardée et la vélocité de détorsion diastolique a atteint son maximum plus tard durant la diastole chez les patients ayant un choc septique que chez les volontaires en santé (104 ± 16 % vs 111 ± 14 % et 13 ± 5 % vs 21 ± 10 %; P = 0,03 et P = 0,034, respectivement). L'épreuve de remplissage a augmenté la torsion maximale dans les deux groupes (choc septique, 10,2 ± 5,3 vs 12,6 ± 3,9; volontaires en santé, 16,3 ± 4,5 vs 18,1 ± 6; P = 0,01). L'épreuve de remplissage a augmenté le volume d′éjection systolique du ventricule gauche chez les patients ayant un choc septique (P = 0,003).
Comparativement aux volontaires en santé, la torsion ventriculaire gauche est réduite chez les patients ayant un choc septique. Le remplissage atténue les anomalies de la torsion parallèlement à l'augmentation du volume d′éjection systolique. La réduction du mouvement de torsion pourrait être une composante pertinente de la cardiomyopathie septique. C'est une notion qui mérite d'autres études chez de plus vastes populations.
The Canadian journal of cardiology 01/2013; 29(12):1665–1671. · 3.12 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: AIM OF THE STUDY: To evaluate the association between haemodynamic variables during the first 24hours after intensive care unit (ICU) admission and neurological outcome in out-of-hospital cardiac arrest (OHCA) victims undergoing therapeutic hypothermia. METHODS: In a multi-disciplinary ICU, records were reviewed for comatose OHCA patients undergoing therapeutic hypothermia. The hourly variable time integral of haemodynamic variables during the first 24hours after admission was calculated. Neurologic outcome was assessed at day 28 and graded as favourable or adverse based on the Cerebral Performance Category of 1-2 and 3-5. Bi- and multivariate regression models adjusted for confounding variables were used to evaluate the association between haemodynamic variables and functional outcome. RESULTS: 67/134 patients (50%) were classified as having favourable outcome. Patients with adverse outcome had a higher mean heart rate (73 [62-86] vs. 66 [60-78] bpm; p=0.04) and received noradrenaline more frequently (n=17 [25.4%] vs. n=9 [6%]; p=0.02) and at a higher dosage (128 [56-1004] vs. 13 [2-162] μg/h; p=0.03) than patients with favourable outcome. The mean perfusion pressure (mean arterial blood pressure minus central venous blood pressure) (OR=1.001, CI 95=1-1.003; p=0.04) and cardiac index time integral (OR=1.055, CI 95=1.003-1.109; p=0.04) were independently associated with adverse outcome at day 28. CONCLUSION: Mean perfusion pressure and cardiac index during the first 24hours after ICU admission were weakly associated with neurological outcome in an OHCA population undergoing therapeutic hypothermia. Further studies need to elucidate whether norepinephrine-induced increases in perfusion pressure and cardiac index may contribute to adverse neurologic outcome following OHCA.