Joana Silvestre

Impact of fulminant hepatic failure in C-reactive protein?

INTRODUCTION Fulminant hepatic failure (FHF) refers to the rapid development of severe acute liver injury with impaired synthetic function, coagulopathy, and encephalopathy in a person who previously had a normal liver or had a well-compensated liver disease. It is a rare complication in critically ill patients and carries a very bad prognosis. Serum C-reactive protein (CRP), a useful marker of infection, is produced exclusively by the liver. AIM The aim of this study was to assess CRP concentrations in patients with FHF. METHODS We prospectively identified patients with sepsis and FHF treated at the intensive care unit (ICU). Data collected included admission diagnosis, medical history, systemic inflammatory response syndrome criteria, Acute Physiologic and Chronic Health Evaluation II, and Sequential Organ Failure Assessment scores. C-reactive protein and white cell count were measured at admission and then daily until ICU discharge. RESULTS We included 7 patients with FHF and sepsis. Six patients died with severe multiple organ failure. Six patients were already admitted with FHF, with the remaining one being diagnosed at the 26th day of ICU stay. All patients present severe coagulopathy. In all septic patients, despite clinical deterioration, CRP levels were markedly decreased sometimes reaching undetectable levels. CONCLUSION In septic patients with FHF, CRP is more a marker of severe liver dysfunction and should not be used as a marker of infection. As a result, in a patient admitted with a very high suspicion of infection and an abnormally low CRP concentration or with a marked CRP decline despite persistent septic shock, severe hepatic failure should be ruled out.

Metformin-induced lactic acidosis: a case series

IntroductionUnlike other agents used in the treatment of type 2 diabetes mellitus, metformin has been shown to reduce mortality in obese patients. It is therefore being increasingly used in higher doses. The major concern of many physicians is a possible risk of lactic acidosis. The reported frequency of metformin related lactic acidosis is 0.05 per 1000 patient-years; some authors advocate that this rate is equal in those patients not taking metformin.Case presentationWe present two case reports of metformin-associated lactic acidosis. The first case is a 77 year old female with a past medical history of hypertension and type 2 diabetes mellitus who had recently been prescribed metformin (3 g/day), perindopril and acetylsalicylic acid. She was admitted to the emergency department two weeks later with abdominal pain and psychomotor agitation. Physical examination revealed only signs of poor perfusion. Laboratory evaluation revealed hyperkalemia, elevated creatinine and blood urea nitrogen and mild leukocytosis. Arterial blood gases showed severe lactic acidemia. She was admitted to the intensive care unit. Vasopressor and ventilatory support was initiated and continuous venovenous hemodiafiltration was instituted. Twenty-four hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the sixth day. The second patient is a 69 year old male with a past medical history of hypertension, type 2 diabetes mellitus and ischemic heart disease who was on metformin (4 g/day), glycazide, acetylsalicylic acid and isosorbide dinitrate. He was admitted to the emergency department in shock with extreme bradycardia. Initial evaluation revealed severe lactic acidosis and elevated creatinine and urea. The patient was admitted to the Intensive Care Unit and commenced on continuous venovenous hemodiafiltration in addition to other supportive measures. A progressive recovery was observed and he was discharged from the intensive care unit on the seventh day.ConclusionWe present two case reports of severe lactic acidosis most probably associated with high doses of metformin in patients with no known contraindications for metformin prescription. In both patients no other condition was identified to cause such severe lactic acidosis. Although controversial, lactic acidosis should be considered in patients taking metformin.

Should C-reactive protein concentration at ICU discharge be used as a prognostic marker?

BackgroundAbout one third of hospital mortality in critically ill patients occurs after Intensive Care Unit (ICU) discharge. Some authors have recently hypothesized that unresolved or latent inflammation and sepsis may be an important factor that contributes to death following successful discharge from the ICU.AimThe aim of our study was to determine the ability of the clinical and inflammatory markers at ICU discharge to predict post-ICU mortality.MethodsA prospective observational cohort study was conducted during a 14-month period in an 8 bed polyvalent ICU. Acute Physiology and Chronic Health Evaluation (APACHE) II score, Simplified Acute Physiology Score (SAPS) II, Sequential Organ Failure Assessment (SOFA) score, Therapeutic Intervention Scoring System-28 (TISS-28), C-reactive protein (CRP), white cell count (WCC) and body temperature of the day of ICU discharge were collected from patients who survived their first ICU admission.ResultsDuring this period 156 patients were discharged alive from the ICU. A total of 29 patients (18.6%) died after ICU discharge. There were no differences in clinical and demographic characteristics between survivors and nonsurvivors. C-reactive protein levels at ICU discharge were not significantly different between survivors and nonsurvivors. The area under receiver operating characteristics curves of APACHE II, SAPS II, SOFA, TISS-28, CRP, WCC and body temperature at ICU discharge as prognostic markers of hospital death were 0.76 (95% confidence interval (CI) 0.67-0.86); 0.75 (95% CI 0.66-0.85); 0.72 (95% CI 0.62-0.83); 0.64 (95% CI 0.52-0.77); 0.55 (95% CI 0.43-0.67); 0.55 (95% CI 0.42-0.66) and 0.54 (95% CI 0.44-0.67) respectively. The hospital mortality rate of the patients with CRP <5, 5-10, >10 mg/dL was 15.1%, 16.1% and 33.3% respectively (p = NS).ConclusionsAt ICU discharge serum CRP concentration was a poor marker of post-ICU prognosis. Post-ICU death appears to be unrelated to the persistent inflammatory response.

Infeção por staphylococcus aureus meticilina-resistente da comunidade em Portugal

Methicillin-resistant Staphylococcus aureus (MRSA) has recently emerged as a cause of community-acquired infections among individuals without risk factors. Community-associated MRSA (CA-MRSA) appears to be more virulent, causing superficial mild skin and soft tissue infections to severe necrotizing fasciitis, and in rare cases, pneumonia. Community-associated MRSA was first reported in Australia in the early 80s, after almost two decades in the USA, and then in several countries in Europe, Asia and South America. No data exists in Portugal. We report the first case of CA-MRSA infection in Portugal, in a young adult with severe necrotizing pneumonia, complicated with bilateral empyema and respiratory failure.

Acute bacterial meningitis in the intensive care unit and risk factors for adverse clinical outcomes: retrospective study.

BACKGROUND Bacterial meningitis constitutes a medical emergency. Its burden has driven from childhood to the elderly and the immunocompromised population. However, the admission of patients with bacterial meningitis to the intensive care unit (ICU) has been sparsely approached, as have the prognostic factors associated with an adverse clinical outcome. METHODS We performed a retrospective analysis during a 7-year period of patients older than 18 years admitted to 2 polyvalent ICUs. Clinical, demographic, and outcome data were collected to evaluate its clinical impact on the outcome of patients with acute bacterial meningitis. RESULTS We identified 65 patients with the diagnosis of acute bacterial meningitis (mean Acute Physiology and Chronic Health Evaluation II, 23; hospital mortality, 40%). Upon clinical presentation, their most frequent signs were fever (84%), seizures (21.5%), and a low Glasgow Coma Scale (GCS) score (GCS<8; 58.4%). Fifty-five patients (85%) required organ support. A definite microbiological diagnosis was achieved in 45 patients. An adverse clinical outcome was noted in 46 patients (71%). These patients were older (P=.005), had higher Physiology and Chronic Health Evaluation II score (P=.022), and had lower GCS (P=.022). In the multivariate analysis, older age (per year; adjusted odds ratio [aOR], 1.059) was associated with an adverse outcome, whereas a higher GCS (per point; aOR, 0.826) and presence of fever upon admission (aOR, 0.142) increase the chance of a good recovery. CONCLUSIONS Patients with acute bacterial meningitis admitted to ICU had substantial morbidity and mortality. Those with low GCS or absence of fever have a particularly high risk of an adverse outcome.

Paraneoplastic necrotizing myopathy in a woman with breast cancer: a case report.

IntroductionParaneoplastic necrotizing myopathy is a rare disorder, described as a proximal, symmetrical, and rapidly progressing myopathy that is manifested as a paraneoplastic syndrome. Diagnosis is established via histological examination of the muscle biopsy.Case presentationWe present the case of a 53-year-old woman, born in Guinea-Bissau, with a history of locally advanced breast cancer, diagnosed ten months previously. The patient had experienced a progressively proximal muscle weakness of the lower extremities, which led to a total inability to walk. Upon neurological examination, the patient showed muscle weakness and atrophy in both proximal lower extremities without myalgia. Muscle strength was graded according to the Medical Research Council Scale as 2 out of 5 in the bilateral iliopsoas muscle, and 4 out of 5 in the bilateral quadriceps femoris. The deep-tendon reflexes were hypoactive. The laboratory examination showed increased values of serum creatinine kinase and myoglobin. An electromyogram showed an incomplete interference pattern during voluntary contraction in the iliopsoas and quadriceps femoris. The motor nerve conduction was 44.1 m/s and 44.3 m/s in the right and left tibial nerves, respectively, and 46.5 m/s and 46.1 m/s in the right and left peroneal nerves, respectively. The sensory motor nerve conductions and the compound motor action potential amplitudes were normal. These findings, despite not being specific, suggested a myopathy. Consequently, a muscle biopsy was performed. A biopsy specimen showed myopathic changes that were characteristic of a necrotizing myopathy.ConclusionTreatment for this syndrome consists of controlling the tumor, and providing corticoid therapy. This led to the partial remission of the neurological manifestations.

Assessment of risk factors for in-hospital mortality after intensive care unit discharge

Context: Post-intensive care unit (ICU) mortality predictors are unknown. Objective: To assess post-ICU in-hospital mortality predictors. Materials and methods: Analysis of 296 patients discharged alive from a medical-surgical ICU during an 18-month period. Results: Post-ICU in-hospital mortality was 22.6%. Nonsurvivors had significantly higher Charlson comorbidity score and more often had a tracheostomy. C-reactive protein (CRP) “alert measurement”, ≥ 6 mg/dL, independently discriminated survivors from nonsurvivors. Discussion: A CRP “alert measurement” or the need for tracheostomy may be used to identify patients with high risk of dying after ICU discharge. Conclusions: Charlson comorbidity score, CRP and tracheostomy predicted post-ICU in-hospital mortality.

Severe diltiazem poisoning treated with hyperinsulinaemia-euglycaemia and lipid emulsion.

Introduction. Calcium channel blockers (CCBs) drugs are widely used in the treatment of cardiovascular diseases. CCB poisoning is associated with significant cardiovascular toxicity and is potentially fatal. Currently, there is no specific antidote and the treatment of CCB poisoning is supportive; however, this supportive therapy is often insufficient. We present a clinical case of severe diltiazem poisoning and the therapeutic approaches that were used. Case Report. A 55-year-old male was admitted to the intensive care unit (ICU) after voluntary multiple drug intake, including extended release diltiazem (7200 mg). The patient developed symptoms of refractory shock to conventional therapy and required mechanical ventilation, a temporary pacemaker, and renal replacement therapy. Approximately 17 hours after drug intake, hyperinsulinaemia-euglycaemia with lipid emulsion therapy was initiated, followed by progressive haemodynamic recovery within approximately 30 minutes. The toxicological serum analysis 12 h after drug ingestion revealed a diltiazem serum level of 4778 ng/mL (therapeutic level: 40–200 ng/mL). Conclusions. This case report supports the therapeutic efficacy of hyperinsulinaemia-euglycaemia and lipid emulsion in the treatment of severe diltiazem poisoning.

Exertional heat stroke and acute liver failure: a late dysfunction.

Heat stroke (HS) is defined as a severe elevation of core body temperature along with central nervous system dysfunction. Exertional heat stroke (EHS) with acute liver failure (ALF) is a rare condition. The authors report the case of a 25-year-old man with a history of cognitive enhancers’ intake who developed hyperthermia and neurological impairment while running an outdoor marathon. The patient was cooled and returned to normal body temperature after 6 h. He subsequently developed ALF and was transferred to the intensive care unit. Over-the-counter drug intake may have been related to heat intolerance and contributed to the event. The patient was successfully treated with conservative measures. In the presence of EHS, it is crucial to act promptly with aggressive total body cooling, in order to prevent progression of the clinical syndrome. Liver function must also be monitored, since it can be a late organ dysfunction.

Biomarkers kinetics in the assessment of ventilator-associated pneumonia response to antibiotics - results from the BioVAP study

Purpose: Our aim was to evaluate the role of biomarker kinetics in the assessment of ventilator‐associated pneumonia (VAP) response to antibiotics. Materials and methods: We performed a prospective, multicenter, observational study to evaluate in 37 microbiologically documented VAP, the kinetics of C‐reactive protein (CRP), procalcitonin (PCT), mid‐region fragment of pro‐adrenomedullin (MR‐proADM). The kinetics of each variable, from day 1 to 6 of therapy, was assessed with a time dependent analysis comparing survivors and non‐survivors. Results: During the study period kinetics of CRP as well as its relative changes, CRP‐ratio, was significantly different between survivors and non‐survivors (p = 0.026 and p = 0.005, respectively). On day 4 of antibiotic therapy, CRP of survivors was 47% of the initial value while it was 96% in non‐survivors. The kinetics of other studied variables did not distinguish between survivors and non‐survivors. In survivors the bacterial load also decreased markedly. Adequate initial antibiotic therapy was associated with lower mortality (p = 0.025) and faster CRP decrease (p = 0.029). Conclusions: C‐reactive protein kinetics can be used to identify VAP patients with poor outcome as soon as four days after the initiation of treatment. (Trial registration ‐ NCT02078999; registered 3 August 2012). HIGHLIGHTSBiomarkers could be useful in the assessment of VAP response to antibiotics.Among the studied biomarkers CRP and CRP‐ratio showed the best performance.CRP course showed a good correlation with the adequacy of antibiotic therapy.CRP course showed a good correlation with the tracheal bacterial load.