Scott H. Norwood

OBJECTIVE: To determine the incidence of tracheal stenosis, voice and breathing changes, and stomal complications after percutaneous dilatational tracheostomy (PDT). METHODS: From December 1992 through June 1999, 420 critically ill patients underwent 422 PDTs. There were 340 (81%) long-term survivors, 100 (29%) of whom were interviewed and offered further evaluation by fiberoptic laryngotracheoscopy (FOL) and tracheal computed tomography (CT). Tracheal stenosis was defined as more than 10% tracheal narrowing on transaxial sections or coronal and sagittal reconstruction views. Forty-eight patients agreed to CT evaluation; 38 patients also underwent FOL. CT and FOL evaluations occurred at 30 +/- 25 (mean +/- standard deviation) months after PDT. RESULTS: Twenty-seven (27%) patients reported voice changes and 2 (2%) reported persistent severe hoarseness. Vocal cord abnormalities occurred in 4/38 (11%) patients, laryngeal granuloma in 1 (3%) patient, focal tracheal mucosal erythema in 2 (5%) patients, and severe tracheomalacia/stenosis in 1 (2.6%) patient. CT identified mild (11-25%) stenosis in 10 (21%) asymptomatic patients, moderate (26-50%) stenosis in 4 (8.3%) patients, 2 who were symptomatic, and severe (>50%) stenosis in 1 (2%) symptomatic patient. Ten patients (10%) reported persistent respiratory problems after tracheal decannulation, but only four agreed to be studied. Two patients had moderate stenosis, and one had severe stenosis. One patient's CT scan was normal. No long-term stomal complications were identified or reported. CONCLUSIONS: Subjective voice changes and tracheal abnormalities are common after endotracheal intubation followed by PDT. Long-term follow-up of critically ill patients identified a 31% rate of more than 10% tracheal stenosis after PDT. Symptomatic stenosis manifested by subjective respiratory symptoms after decannulation was found in 3 of 48 (6%) patients.

BACKGROUND: Patients with traumatic intracranial hemorrhagic injuries (IHIs) are at high risk for venous thromboembolism (VTE). The safety of early anticoagulation for IHI has not been established. HYPOTHESIS: Enoxaparin can be safely administered to most patients with IHI for VTE prophylaxis. SETTING: Level I trauma center. DESIGN: Prospective, single-cohort, observational study. PATIENTS AND METHODS: One hundred fifty (85%) of 177 patients with blunt IHI received enoxaparin beginning approximately 24 hours after hospital admission until discharge. Brain computed tomographic (CT) scans were performed at admission, 24 hours after admission, and at variable intervals thereafter based on clinical course. Patients were excluded for coagulopathy, heparin allergy, expected brain death or discharge within 48 hours, and age younger than 14 years. Complications of enoxaparin prophylaxis were defined as Marshall CT grade progression of IHI, expansion of an existing IHI, or development of a new hemorrhagic lesion on follow-up CT after beginning enoxaparin use. RESULTS: Thirty-four patients (23%) had CT progression of IHI. Twenty-eight CT scans (19%) worsened before enoxaparin therapy and 6 (4%) worsened after beginning enoxaparin use. No differences between operative patient (2/24, 8%) and nonoperative patient (4/126, 3%) complications were identified (P =.23). Study group mortality was 7% (10/150). All 6 patients who developed progression of IHI after initiation of enoxaparin therapy survived hospitalization. A deep vein thrombosis was identified in 2 (2%) of 106 patients. CONCLUSION: Enoxaparin can be safely used for VTE prophylaxis in trauma patients with IHI when started 24 hours after hospital admission or after craniotomy.

Several temporary abdominal wall closure techniques have been described in the literature. We present our experience with an inexpensive and efficient method of temporary abdominal closure when bowel edema and distension preclude safe primary closure. Our technique is a variation of the silon (silo) closure used in the repair of gastroschisis and omphalocele, using a pre-gas-sterilized, soft 3-L plastic cystoscopy fluid irrigation bag cut to an oval shape and stapled or sutured to the skin edges of the wound.

BACKGROUND: Blunt cerebrovascular injuries (BCVI) are rare but potentially devastating injuries, particularly if the diagnosis is delayed. Only four-vessel cerebral angiography (FVCA) has been shown to be adequately sensitive and specific as a screening tool for BCVI but is resource-intensive and invasive. Computed tomography (CT) angiography has emerged as a possible alternative, but its accuracy has been poor, particularly for low-grade injuries. Recent advances in CT technology, particularly the use of a multi-detector array for image acquisition should improve the accuracy of this technique. This study is the first reported experience of the role of the 16-slice multi- detector CT scanner in screening for BCVI. METHODS: From January 2, 2003 to October 31, 2004, all patients who met predefined screening criteria were screened for blunt injury to the carotid (BCI) and vertebral (BVI) arteries with a 16-slice multi-detector CT scanner with angiographic reconstruction (CTA). If CTA was positive or equivocal for BCVI, FVCA was performed as a confirmatory test. If CTA was negative, no further diagnostic studies were performed. RESULTS: There were 435 patients who met criteria and were screened with CTA. Of these, 25 injuries were identified in 24 patients for an incidence of BCVI of 1.2% (24/2023) among all blunt admissions (BTA) and 5.5% (24/435) among screened patients (SP). This was increased compared with the four-slice era (0.38% BTA, 2.4% SP, p<0.01). No patient with a negative CTA was subsequently identified as having, or developed neurologic symptoms attributable to a missed BCVI. CONCLUSION: Sixteen-slice multi-detector CT angiography is an excellent tool to screen for BCVI and detects all clinically significant injuries. The detected incidence of BCVI increased more than threefold with the 16-slice scanner when compared with the four-slice scanner. This demonstrates a clear technological improvement in our ability to screen for these injuries.

BACKGROUND: Blunt cerebrovascular injuries are rare injuries causing substantial morbidity and mortality. The appropriate screening methods and treatment options for these injuries are controversial. We examined our experience with these injuries at a community Level I Trauma center over a 51 month period. STUDY DESIGN: A retrospective review and analysis was done of all patients with the diagnosis of a blunt cerebrovascular injury during this period. RESULTS: Fourteen patients had blunt carotid injury (0.40%) and three had blunt vertebral injury (0.09%) out of 3,480 total blunt admissions. The overall incidence of blunt cerebrovascular injury was 0.49%. The most common associated injuries were to the head (59%) and chest (47%) regions. The overall mortality rate was 59% (10 of 17), with death occurring in 8 of 14 (57%) blunt carotid injury patients and 2 of 3 (67%) blunt vertebral injury patients. Eight of ten (80%) deaths were directly attributable to the blunt cerebrovascular injury. Median time until diagnosis was 12.5 h (range 1-336 h) for the entire group and 19.5 h for nonsurvivors. Diagnosis was delayed > 24h in 7 patients and > 48h in 5 patients. All five patients whose diagnoses were delayed > 48 h developed complications, and four (80%) of these patients died. CONCLUSIONS: Blunt cerebrovascular injury is uncommon, but lethal; particularly when the diagnosis is delayed. Aggressive screening protocols based on mechanism of injury, associated injuries, and physical findings are justified to minimize morbidity and mortality. Head and chest injuries may serve as markers for blunt cerebrovascular injury. Most deaths are directly attributable to the blunt cerebrovascular injury and not to associated injuries.