Autopsies of sudden infant death syndrome—classification and epidemiology

An enquiry into sudden infant death syndrome (SIDS) in 1987 furnished us with detailed epidemiological data for 281 cases that underwent a thorough post-mortem examination. This analysis uses these data to evaluate the role the autopsy plays in explaining sudden death. The cases were classified into three diagnostic groups: explained causes of death (group 1), unexplained deaths with anomalies (group 2), and no anomaly (group 3). These 281 cases show the three essential features that characterize SIDS: over-representation of males, increased deaths during the second and third months of life, and increased deaths during winter. The autopsy examination revealed that many of these deaths had a medical explanation. Almost half were assigned to group 1. At the time of autopsy, no precise pathology could be diagnosed for 147 deaths; of these, 140 showed histological anomalies. There were only seven sudden deaths for which no abnormal sign was evident at the autopsy. These results are compared with those of similar studies and discussed in connection with three factors: the initial selection of cases, the nature and degree of the investigations, and the possible interpretations of the symptoms uncovered.     

Nonpharmacological prevention of hospital-acquired pneumonia

Hospital-acquired pneumonia (HAP) is the most common nosocomial infection occurring among mechanically ventilated patients. The benefits associated with the systematic prevention of HAP include fewer infections with high-risk antibiotic-resistant bacteria, lower rates of hospital mortality, reduced medical care costs, and shorter hospital lengths of stay. Unfortunately, many hospitals do not have an organized approach to the prevention of HAP. This review will describe the nonpharmacological approaches available for the prevention of HAP. It should help clinicians to design their own strategies for the prevention of this important hospital-acquired infection.     

Surveillance for vancomycin-resistant enterococci: type, rates, costs, and implications.

OBJECTIVE: To evaluate 2 active surveillance strategies for detection of enteric vancomycin-resistant enterococci (VRE) in an intensive care unit (ICU). DESIGN: Thirty-month prospective observational study. SETTING: ICU at a university-affiliated referral center. PATIENTS: All patients with an ICU stay of 24 hours or more were eligible for the study. INTERVENTION: Clinical active surveillance (CAS), involving culture of a rectal swab specimen for detection of VRE, was performed on admission, weekly while the patient was in the ICU, and at discharge. Laboratory-based active surveillance (LAS), involving culture of a stool specimen for detection of VRE, was performed on stool samples submitted for Clostridium difficile toxin detection. RESULTS: Enteric colonization with VRE was detected in 309 (17%) of 1,872 patients. The CAS method initially detected 280 (91%) of the 309 patients colonized with VRE, compared with 25 patients (8%) detected by LAS; colonization in 4 patients (1%) was initially detected by analysis of other clinical specimens. Most patients with colonization (76%) would have gone undetected by LAS alone, whereas use of the CAS method exclusively would have missed only 3 patients (1%) who were colonized. CAS cost Dollars 1,913 per month, or Dollars 57,395 for the 30-month study period. Cost savings of CAS from preventing cases of VRE colonization and bacteremia were estimated to range from Dollars 56,258 to Dollars 303,334 per month. CONCLUSIONS: A patient-based CAS strategy for detection of enteric colonization with VRE was superior to LAS. In this high-risk setting, CAS appeared to be the most efficient and cost-effective surveillance method. The modest costs of CAS were offset by the averted costs associated with the prevention of VRE colonization and bacteremia.     

Comment on ‘Predicting recurrence in axillary node negative breast cancer patients’, by Rosner and Lane

on behalf of the Nottingham Breast Unit     

Neural and musculoskeletal contributions to the development of stance balance control in typical children and in children with cerebral palsy

Studies on the development of automatic postural responses in both typically developing children and children with cerebral palsy were performed. With the appearance of "pull-to-stand" behavior, typically developing children first began to show muscle responses to platform movements in mainly the ankle muscles. With increased development, additional agonist muscles were added to the response pattern and a consistent distal to proximal sequence began to emerge. Well-organized responses were seen with the onset of independent stance and walking, along with the reduction of antagonist muscle co-activation. The older children with cerebral palsy who were pre-walkers had immature muscle activation patterns like those seen in the typically developing children at the pull-to- stand stage of development. These included disorganized muscle responses and increased frequency of coactivation of both proximal–distal and agonist–antagonist muscles. In order to determine if musculoskeletal constraints contributed to these response patterns, normal children were asked to stand in a crouched posture similar to that of children with CP. This caused postural muscle response patterns to more closely approximate those of children with spastic diplegia.     

Noncardiogenic pulmonary edema following upper airway obstruction. 7 cases and a review of the literature

Pulmonary edema is a relatively common problem facing most physicians. Its separation into cardiogenic and noncardiogenic or high-permeability variants is crucial to its proper early management. Our understanding of the disease processes producing noncardiogenic pulmonary edema has greatly expanded in the last 2 decades. Upper airway obstruction (UAO) is one of many recently recognized mechanisms which can produce noncardiogenic pulmonary edema. The UAO may be subtle in some patients, making its association with the subsequent pulmonary edema difficult especially for the physician unaware of this entity and the potential risk factors contributing to it. A high index of suspicion for this diagnosis is required in the right clinical settings. Our clinical results support a noncardiogenic basis for pulmonary edema occurring after UAO. Five of our 7 patients had at least 1 identifiable risk factor for the development of peri-intubation UAO and pulmonary edema. Additionally, the onset of pulmonary edema following UAO and the duration of the pulmonary edema varied considerably in our patients. Individuals with additional risk factors for the development of noncardiogenic pulmonary edema developed a more severe form of pulmonary edema associated with other organ-system disease. However, in most individuals, UAO-associated pulmonary edema appears to be a self-limited reversible process once it is recognized and properly treated.     

Dynamic evolution of coagulopathy in the first day of severe sepsis: relationship with mortality and organ failure

OBJECTIVE: To determine whether changes in coagulation biomarkers during the first day of severe sepsis correlate with progression from single to multiple organ failure and subsequent death. DESIGN: Analysis of secondary endpoints in a prospective, randomized, placebo-controlled, multinational clinical trial (PROWESS). SETTING: The study involved 164 medical centers. PATIENTS: A total of 840 patients who met criteria for severe sepsis and were randomized to receive placebo plus supportive care. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Coagulation biomarkers, prothrombin time, antithrombin activity, and D-dimer and protein C levels were measured, and Sequential Organ Failure Assessment was performed daily. Multiple logistic regression analysis identified baseline antithrombin activity <54% and changes in prothrombin time, D-dimer, and antithrombin activity during the first calendar day after the onset of the first sepsis-induced organ dysfunction (i.e., the first day of severe sepsis, day 1) as predictive of 28-day mortality (p < or = .01). A composite coagulopathy score was determined using points for predetermined levels of change from baseline to day 1. The composite coagulopathy score correlated with progression from single to multiple organ failure (p = .0007), time to resolution of organ failure (p = .0004), and 28-day mortality (p < .0001). Combining the composite coagulopathy score with the Acute Physiology and Chronic Health Evaluation (APACHE) II score improved ability to identify patients who would progress to multiple organ failure (area under receiver operating characteristic curve 0.61 APACHE II vs. 0.65 APACHE II + composite coagulopathy score) and who would die (area under receiver operating characteristic curve 0.69 APACHE II vs. 0.74 APACHE II + composite coagulopathy score). CONCLUSIONS: Continuation or worsening of coagulopathy during the first day of severe sepsis was associated with increased development of new organ failure and 28-day mortality. These results further suggest that coagulation abnormalities contribute to organ failure and death.