Predicting the diagnosis of autism in adults using the Autism-Spectrum Quotient (AQ) questionnaire.

BACKGROUND: Many adults with autism spectrum disorder (ASD) remain undiagnosed. Specialist assessment clinics enable the detection of these cases, but such services are often overstretched. It has been proposed that unnecessary referrals to these services could be reduced by prioritizing individuals who score highly on the Autism-Spectrum Quotient (AQ), a self-report questionnaire measure of autistic traits. However, the ability of the AQ to predict who will go on to receive a diagnosis of ASD in adults is unclear. METHOD: We studied 476 adults, seen consecutively at a national ASD diagnostic referral service for suspected ASD. We tested AQ scores as predictors of ASD diagnosis made by expert clinicians according to International Classification of Diseases (ICD)-10 criteria, informed by the Autism Diagnostic Observation Schedule-Generic (ADOS-G) and Autism Diagnostic Interview-Revised (ADI-R) assessments. RESULTS: Of the participants, 73% received a clinical diagnosis of ASD. Self-report AQ scores did not significantly predict receipt of a diagnosis. While AQ scores provided high sensitivity of 0.77 [95% confidence interval (CI) 0.72-0.82] and positive predictive value of 0.76 (95% CI 0.70-0.80), the specificity of 0.29 (95% CI 0.20-0.38) and negative predictive value of 0.36 (95% CI 0.22-0.40) were low. Thus, 64% of those who scored below the AQ cut-off were 'false negatives' who did in fact have ASD. Co-morbidity data revealed that generalized anxiety disorder may 'mimic' ASD and inflate AQ scores, leading to false positives. CONCLUSIONS: The AQ's utility for screening referrals was limited in this sample. Recommendations supporting the AQ's role in the assessment of adult ASD, e.g. UK NICE guidelines, may need to be reconsidered.

Are temporary inferior vena cava filters really temporary?

BACKGROUND: Despite significant risk for venous thromboembolism, severely injured trauma patients often are not candidates for prophylaxis or treatment with anticoagulation. Long-term inferior vena cava (IVC) filters are associated with increased risk of postphlebitic syndrome. Retrievable IVC filters potentially offer a better solution, but only if the filter is removed; our hypothesis is that the most of them are not. METHODS: This retrospective study queried a level I trauma registry for IVC filter insertion from September 1997 through June 2004. RESULTS: One IVC filter was placed before the availability of retrievable filters in 2001. Since 2001, 27 filters have been placed, indicating a change in practice patterns. Filters were placed for prophylaxis (n = 11) or for therapy in patients with pulmonary embolism or deep vein thrombosis (n = 17). Of 23 temporary filters, only 8 (35%) were removed. CONCLUSIONS: Surgeons must critically evaluate indications for IVC filter insertion, develop standard criteria for placement, and implement protocols to ensure timely removal of temporary IVC filters.

Thrombohemolytic thrombocytopenic purpura during penicillamine therapy.

Penicillamine therapy was associated with the development of thrombohemolytic thrombocytopenic purpura (TTP) in a 23-year-old woman. The immunological and hematological toxicity of penicillamine, as well as the occurrence of TTP with parent penicillin compounds, indicates a probable etiological role of this drug.

Lazaroids prevent acute cyclosporine-induced renal vasoconstriction.

BACKGROUND: Cyclosporine (CsA)-induced nephrotoxicity may be due to intrarenal vasoconstriction and glomerular hypoperfusion. Several factors, including endothelin and prostanoids, are suggested mediators of this response. Recent evidence suggests that CsA leads to increased oxygen-derived free radical (ODFR) production and lipid peroxidation in renal tissue. Whether this leads to alterations in renal vessel reactivity is unclear. Lazaroids, such as U74389G, are radical-quenching antioxidants that inhibit ODFR-induced lipid peroxidation and may improve renal function after ischemia and reperfusion. We hypothesized that ODFRs contribute to CsA-induced alterations of the renal microcirculation. METHODS: Rat hydronephrotic kidneys were studied by video microscopy. Interlobular arteriolar diameter and flow, afferent and efferent arteriolar diameters, and cardiac output were measured at 15-min intervals for 120 min. U74389G or its vehicle was infused 15 min before topical application of CsA to the kidney. The results were compared with U74389G alone and normal saline. RESULTS: CsA administration caused renal microvascular vasoconstriction (10-25% below baseline) and hypoperfusion (35% below baseline). Both vasoconstriction and hypoperfusion were significantly attenuated by U74389G (5-8% and 20% below baseline, respectively). CONCLUSIONS: Inhibition of lipid peroxidation by U74389G maintained renal blood flow during acute CsA administration. These data suggest that ODFRs are involved in the renal microvascular response to CsA. Inhibition of ODFR-induced lipid peroxidation may help prevent CsA-induced glomerular hypoperfusion. Lazaroids may prove an effective adjunct in reducing CsA-induced nephrotoxicity.

Differential microvascular response to cyclooxygenase blockade in the rat small intestine during acute bacteremia.

To determine whether arachidonic acid metabolites are mediators of regional blood flow changes during sepsis, we examined the effects of cyclooxygenase blockade on intestinal microvascular diameters and blood flow during acute bacteremia, induced in the rat by the intravenous injection of 10(9) live Escherichia coli. Mean arterial pressure, cardiac output, intestinal microvascular diameters, and blood flow were measured in the presence or absence of a topically applied selective cyclooxygenase inhibitor (mefenamate). Bacteremia caused a diffuse constriction of both arterioles and venules and a concomitant 50% decrease in blood flow. Treatment with mefenamate did not affect baseline intestinal microvascular tone or bacteremia-induced arteriolar constriction and hypoperfusion, but did reverse an intense venular constriction. Our results suggest that the small intestinal microcirculation has a differential response to cyclooxygenase products of arachidonic acid metabolism during acute bacteremia. They appear not to be mediators of the intestinal arteriolar constriction and hypoperfusion observed during acute E. coli bacteremia, but profoundly influence the mesenteric venular constriction. These observations support the concept that microvascular control mechanisms are different not only between but within organ specific vascular beds.

Role of nitric oxide in the small intestinal microcirculation during bacteremia.

Nitric oxide (NO) is an important mediator of the hemodynamic effects of sepsis; however, its microcirculatory effects are unknown. To determine the role of NO in the small intestinal (SI) microcirculation, an intact SI loop was exteriorized from decerebrate rats into a controlled Krebs' bath. Bacteremic rats received 10(9) Escherichia coli intravenously. Videomicroscopy was used to measure arteriolar diameters (A1, A3) and optical Doppler velocimetry to quantitate flow. In controls, topical NO synthase (NO-S) substrate L-arginine (L-ARG; 10(-4) M) did not affect diameters or flow. Inhibition of NO-S by N omega-nitro-L-arginine methyl ester (L-NAME; 10(-4) M) caused constriction (A1 = -18%; A3 = -24% from baseline diameter) and reduced A1 flow by 62%. These alterations were similar to bacteremic controls (A1 = -20%; A3 = -18%; A1 flow = -42%), despite the increased cardiac output (+21%). L-NAME treatment of bacteremic rats resulted in further constriction (A1 = -31%; A3 = -32%) and decreased A1 flow (-75%). Topical L-ARG (10(-4) M) ameliorated constriction (A1 = -6%; A3 = +7%) and improved blood flow (-5%) during bacteremia. We conclude that: 1) NO is important for basal SI microvascular tone; 2) bacteremia causes SI arteriolar constriction and hypoperfusion; 3) NO-S inhibition during sepsis may exacerbate SI vasoconstriction and hypoperfusion.

Progressive decrease in constrictor reactivity of the non-absorbing intestine during chronic sepsis.

Chronic sepsis leads to an impaired intestinal microcirculation, which might reflect altered microvascular control. We hypothesized that intestinal microvascular sensitivity to norepinephrine (NE) is decreased during chronic sepsis. Chronic sepsis was induced by a polymicrobial inoculation of implanted subcutaneous sponges in rats. Septic rats were studied either 24 or 72 h after a single inoculation (1-hit) of bacteria. Other rats received a second inoculation (2-hit) of bacteria 48 h later and were studied at 24 h after the second inoculation. NE (0.01-1.0 microM) responses in the non-absorbing terminal ileal arterioles (inflow A1, proximal-p and distal-d premucosal A3) were measured by video microscopy. NE threshold sensitivity (pD(T20) = -log of 20% response dose) was analyzed. pD(T20) was significantly decreased in A1, pA3, and dA3 of 1-hit 24-h septic rats (P < 0.05), and was further decreased in all vessels of 2-hit 72-h septic rats (P < 0.05). In contrast, the pDT(T20) of all three vessels significantly returned toward normal values after 72 h in rats that had only 1 bacteria inoculation. We conclude that an initial bacterial challenge decreases vasoconstrictor reactivity of the intestinal microcirculation and that subsequent repeated bacterial challenge exacerbates this defect in vasoconstrictor control in the non-absorbing intestine.

Selective microvascular endothelial cell dysfunction in the small intestine following resuscitated hemorrhagic shock.

Following resuscitation (RES) from hemorrhagic shock (HEM), intestinal microvessels develop progressive vasoconstriction that impairs mucosal blood flow, despite central hemodynamic RES. These events might have clinical consequences secondary to occult intestinal ischemia. We hypothesized that the microvascular impairments were due to progressive endothelial cell dysfunction and an associated reduction in the dilator, nitric oxide (NO), following HEM/RES. Male Sprague-Dawley rats, were monitored for central hemodynamics and the terminal ileum was studied with in vivo videomicroscopy. HEM was 50% of baseline mean arterial pressure (MAP) for 60 min, and RES was with shed blood + 1 volume of normal saline (NS). Following HEM/RES, acetylcholine (10)(-7), 10(-5) M) was topically applied and ileal inflow (A1) and premucosal arteriolar diameters were measured to assess endothelial-cell function at 60 and 120 min post-RES. Normalization of MAP, cardiac output, and heart rate demonstrated adequate systemic resuscitation. Post-RES vasoconstriction developed in A1 (-25%) and premucosal (-28%) arterioles with an associated reduction in A1 flow (-47%). However, there was a selective impairment of endothelial-dependent dilation that was manifested only in the smaller premucosal arterioles and not in the inflow, A1 arterioles. This suggests that multiple mechanisms are involved in the development of the post-RES vasoconstriction. The premucosal response was likely mediated by endothelial cell dysfunction, while the A1 response was probably the result of enhanced vasoconstrictor forces. This early microvascular dysfunction might contribute to the late sequelae of intestinal ischemia and might alter microvascular responses to subsequent systemic insults.

Endothelin-1 expression in the small intestine during chronic peritonitis.

Endothelins (ET) have been demonstrated to mediate intestinal microvascular constriction during acute Escherichia coli bacteremia, however, their role during chronic infection is unknown. The purpose of this study was to determine whether ET-1 is synthesized in the small intestine in a more chronic peritonitis model. ET-1 mRNA levels of the terminal ileum in mice following cecal ligation and puncture (CLP) were compared to sham-operated animals and normal unoperated animals. ET gene expression was analyzed using differential reverse transcriptase chain reaction (RT-PCR) with co-amplification of beta-actin as an internal standard. To assess ET peptide expression, serum and intestinal tissue levels were measured using a specific enzyme immunoassay (ELISA). The pattern of ET-1 gene expression post-CLP with a single puncture of the cecum with a 23 ga. needle demonstrated a 3.6-fold increase at 8 h, and a return to sham levels by 24 h (374 +/- 64% at 8 h, p < .05, 128 +/- 13%). An increase of mRNA levels at 24 h post-CLP was observed with a double puncture with an 18 ga. needle (230 +/- 36%, p < .05) accompanied by an increase in serum ET levels (270 +/- 31%, p < .05) and higher tissue ET levels. These data indicate a time-dependent response of ET-1 gene expression in the terminal ileum post-CLP which is related to severity of infection.

Preoperative issues in clinical nutrition.

Allowing a patient's nutritional state to deteriorate through the perioperative period adversely affects measureable outcome related to nosocomial infection, multiple organ dysfunction, wound healing, and functional recovery. Careful preoperative nutritional assessment should include a determination of the level of stress, an evaluation of the status of the GI tract, and the development of specific plans for securing enteral access. Patients already demonstrating compromise of nutritional status (defined by > 10% weight loss and serum albumin level < 2.5 g/dL) should be considered for a minimum of 7 to 10 days of nutritional repletion prior to surgery. Widespread use of total parenteral nutrition in unselected patients is unwarranted, may actually worsen outcome, and should be reserved for preoperative nutritional support only in severely malnourished patients in whom the GI tract is unavailable. Compared with the parenteral route, use of perioperative enteral feeding has been shown to provide more consistent and beneficial results, and can be expected to promote specific advantages in long-term morbidity and mortality.

Nitric oxide synthase inhibition exacerbates sepsis-induced renal hypoperfusion.

BACKGROUND: Hyperdynamic sepsis is often complicated by renal dysfunction, caused in part by renal vasoconstriction and impaired blood flow. Nitric oxide (NO) is an important mediator of hemodynamic responses to sepsis; however, its importance in the renal microcirculation during sepsis is unknown. Our purpose was to determine the role of NO in the renal microcirculation during bacteremia. METHODS: In vivo videomicroscopy was used to study the microcirculation in five groups of hydronephrotic rat kidneys. Cardiac output (CO), mean arterial pressure, interlobular artery (ILA) diameter and flow, and afferent (AFF) and efferent arteriole diameters were measured. RESULTS: NO synthase inhibition in normal rats resulted in hypertension, decreased CO, selective preglomerular constriction (ILA, -21%; AFF, -26% of baseline), and hypoperfusion (-56%). Escherichia coli resulted in a normotensive, high CO state (+23%) with ILA (-25%) and AFF (-20%) constriction and hypoperfusion (-60%). NO synthase inhibition during bacteremia normalized CO and increased mean arterial pressure (+34%) but exacerbated constriction (ILA, -45%; AFF, -33%) and further impaired flow (-90%). CONCLUSIONS: NO maintains preglomerular tone and flow during basal conditions and appears to counteract intrarenal vasoconstrictors during E. coli bacteremia.

Sustained infection induces 2 distinct microvascular mechanisms in the splanchnic circulation.

BACKGROUND: Altered intestinal blood flow during systemic inflammation leads to organ dysfunction. Mucosal ischemia occurs during sepsis despite an increase in portal blood flow. We hypothesized that separate mechanisms are active in the large resistance and small mucosal microvessels to account for this dichotomy. METHODS: Chronic infection was induced in rats by bacterial inoculation (Escherichia coli and Bacteroides fragilis) of an implanted subcutaneous sponge. Separate groups were studied at 24 and 72 hours after a single inoculation of bacterium or 24 hours after a second inoculation (ie, 72 hours of sepsis). Time-matched controls were used for each group. Intravital microscopy of the terminal ileum was used to assess endothelial-dependent vasodilation to acetylcholine (10(-9) to 10(-5) mol/L) in resistance (A(1)) and premucosal (A(3)) arterioles. Threshold sensitivity (-log of 20% response dose) was calculated from dose response curves for each animal. RESULTS: Vasodilator sensitivity to acetylcholine in A(1) arterioles was significantly decreased at 24 hours, and these changes persisted up to 72 hours after a single bacterial inoculation. There was no change in the dilator sensitivity of A(3) arterioles after a single inoculation. When there was a challenge with a second bacterial inoculation, there was a reversal of the A(1) dilator response and an increase in A(3) sensitivity. CONCLUSIONS: An initial septic event results in a decrease in dilator reactivity in the resistance A1 arterioles that persists for at least 72 hours. A sustained septic challenge results in increased dilator reactivity in both A(1) and A(3) vessels. This enhanced sensitivity during sepsis suggests that more than 1 therapeutic approach to preservation of intestinal blood flow will be necessary.

Free radical scavenging by lazaroids improves renal blood flow during sepsis.

BACKGROUND: Acute kidney failure in surgical patients is often related to severe infection. Renal vasoconstriction is a major factor in the genesis of kidney failure. Reactive oxygen species (ROS) are known to mediate kidney injury after ischemia-reperfusion and are increased during sepsis. The role of ROS as mediators of intrarenal vasoconstriction and renal dysfunction during sepsis is unclear. Lazaroids such as U74389G are radical quenching antioxidants that inhibit ROS-induced lipid peroxidation. We sought to determine whether radical scavenging affected the renal microvascular response to a septic challenge. METHODS: In vivo videomicroscopy was used to study the rat hydronephrotic kidney. Interlobular artery (ILA) diameter and flow, afferent and efferent arteriolar diameters, and cardiac output were measured. U74389G or vehicle was infused before a bolus injection of live Escherichia coli or normal saline solution. RESULTS: U74389G alone had no effect on the renal vessels or hemodynamics. E. coli caused preglomerular vasoconstriction (ILA, -32%; afferent, -30% of baseline) and hypoperfusion (-66%) despite increased cardiac output (+54%). U74389G significantly attenuated both the constriction (ILA, -16%; afferent, -9%) and hypoperfusion (-38%) but not increased cardiac output (+41%). CONCLUSIONS: E. coli bacteremia led to preglomerular vasoconstriction and hypoperfusion. Inhibition of lipid peroxidation with the radical scavenger U74389G reduced this effect without altering central hemodynamic responses. Free radicals have a deleterious effect on the renal microcirculation during bacteremia, and these data suggest that antioxidants may be of value in preventing sepsis-associated kidney failure.

Complement inhibition prevents gut ischemia and endothelial cell dysfunction after hemorrhage/resuscitation.

BACKGROUND: Complement, a nonspecific immune response, is activated during hemorrhage/resuscitation (HEM/RES) and is involved in cellular damage. We hypothesized that activated complement injures endothelial cells (ETCs) and is responsible for intestinal microvascular hypoperfusion after HEM/RES. METHODS: Four groups of rats were studied by in vivo videomicroscopy of the intestine: SHAM, HEM/RES, HEM/RES + sCR1 (complement inhibitor, 15 mg/kg intravenously given before resuscitation), and SHAM + sCR1. Hemorrhage was to 50% of mean arterial pressure for 60 minutes followed by resuscitation with shed blood plus an equal volume of saline. ETC function was assessed by response to acetylcholine. RESULTS: Resuscitation restored central hemodynamics to baseline after hemorrhage. After resuscitation, inflow A1 and premucosal A3 arterioles progressively constricted (-24% and -29% change from baseline, respectively), mucosal blood flow was reduced, and ETC function was impaired. Complement inhibition prevented postresuscitation vasoconstriction and gut ischemia. This protective effect appeared to involve preservation of ETC function in the A3 vessels (SHAM 76% of maximal dilation, HEM/RES 61%, HEM/RES + sCR1 74%, P < .05). CONCLUSIONS: Complement inhibition preserved ETC function after HEM/RES and maintained gut perfusion. Inhibition of complement activation before resuscitation may be a useful adjunct in patients experiencing major hemorrhage and might prevent the sequelae of gut ischemia.

Operative strategies for management of abdominal aortic gunshot wounds.

BACKGROUND: Although management of penetrating abdominal trauma has greatly improved, abdominal aortic gunshot wounds (AAGSWs) remain a highly lethal injury. Our experience with AAGSWs was reviewed to define operative strategies that may improve survival. METHODS: Forty-one patients with AAGSWs were treated between 1976 and 1996. Preliminary thoractomy was performed in seven patients. Thirty-nine patients had at least one major associated injury (average, 3.2). RESULTS: Twenty-one patients died. Six of seven patients who underwent preliminary thoracotomy died; all developed coagulopathy, which appeared to contribute to death. Four patients had missed vascular lesions, two of which contributed to their death. Associated injuries are currently managed by "damage control" strategy, in which some injuries are left untreated to focus on hemorrhage control. CONCLUSIONS: We have identified seven operative principles and procedures that we believe may improve survival: (1) thorough knowledge of supraceliac exposure; (2) rapid aortic control at the hiatus rather than by a preliminary thoracotomy; (3) use damage control or abbreviated laparotomy; (4) use packing and mesh closure when coagulopathy and hypothermia are present; (5) primary concern should be cessation of hemorrhage rather than the maintenance of flow; (6) delayed reconstruction using extraanatomic bypass can restore flow; and (7) use angiography to detect missed vascular lesions or problems with vascular repair.

Twelfth rib resection. Preferred therapy for subphrenic abscess in selected surgical patients.

OBJECTIVE: To assess the role of 12th rib resection in the treatment of postoperative, subphrenic abscesses. DESIGN: Consecutive case series. SETTING: University hospital, level I trauma center. PATIENTS: Operative logs for a 13-year period were reviewed for all patients undergoing 12th rib resection for drainage of a postoperative subphrenic abscess. Each individual medical record was reviewed for demographic data, primary diagnosis, computed tomographic scan findings, and clinical status (temperature, white blood cell count, and Acute, Physiologic, Age, and Chronic Health Evaluation II score) at the time of rib resection. MAIN OUTCOME MEASURES: Operative results, microbiological data, complications, and outcomes. RESULTS: Twenty-six patients underwent 27 rib resections for a secondary left subphrenic (23) or a right subhepatic (4) abscess. All patients had undergone at least 1 prior laparotomy (average, 1.5; range, 1-4). Sixteen patients had traumatic injuries, and 7 had complicated pancreatitis. Twelve patients had undergone prior failed attempts at percutaneous drainage before rib resection. Fourteen patients underwent operative drainage without attempted percutaneous drainage, mainly for peripancreatic (7) or multiloculated (3) abscesses. There were 3 postoperative complications (3/27 [11%]): a gastrocutaneous fistula, a gastrocolic-cutaneous fistula requiring laparotomy and temporary colostomy, and fasciitis in the resection site. Four (15%) of the 26 patients died: 3 died of progressive multiple system organ failure, and 1 died of an unrelated injury. The remaining 20 (77%) of the patients were discharged from the hospital with healing wounds and no further episodes of intra-abdominal infection. CONCLUSIONS: Twelfth rib resection is an effective alternative therapy for secondary subphrenic abscesses. The nature of the incision allows for open, dependent drainage; avoids subsequent laparotomy; and effectively controls intra-abdominal infections. Twelfth rib resection remains a useful tool in the treatment of subphrenic abscess and may be the preferred approach when other attempts at abscess drainage have failed.

Haemophilus pneumonia is a common cause of early pulmonary dysfunction following trauma.

BACKGROUND: Haemophilus species are a common cause of community-acquired pneumonia; however, their significance in posttraumatic pneumonia is unclear. DESIGN: Case series. SETTING: University hospital, level I trauma center. PATIENTS: Two hundred fifty-seven consecutive patients with blunt and penetrating trauma treated for pneumonia. MAIN OUTCOME MEASURES: Length of stay in the intensive care unit, duration of ventilatory support, rate of recurrent or persistent pneumonia, and mortality. RESULTS: Ninety-six (37%) of 257 patients treated for pneumonia had a Haemophilus species isolated on sputum culture. Of these 96 patients, 49 (51%) had only Haemophilus species, while 33 (34%) had associated gram-positive organisms and 14 (15%) had gram-negative organisms. Seventeen pure cultures (29%) and seven mixed cultures (15%) (P < .05) were beta-lactamase-positive trains. Compared with patients who had pneumonia caused by other bacteria, patients with Haemophilus species were younger (mean +/- SE, 35 +/- 1.7 vs 42 +/- 1.6 years; P < .05) and more severely injured (Injury Severity Score, 20.7 +/- 1.1 vs 17.5 +/- 0.9; P < .05). There were no differences in any outcome variables between the two groups. Only one (1%) of 96 patients had persistent Haemophilus species on sputum cultures after 7 days of treatment. CONCLUSIONS: Haemophilus species are a frequent cause of pneumonia following traumatic injury. This occurs primarily in the early postinjury phase and therefore should be included in the differential diagnosis of early posttraumatic pulmonary insufficiency.

The role of thoracoscopy in the management of retained thoracic collections after trauma.

BACKGROUND: Retained hemothorax and infected thoracic collections after trauma can be seen in up to 20% of patients initially treated with tube thoracostomy and have traditionally been treated nonoperatively, often with prolonged hospital stays. METHODS: Twenty-five patients with retained thoracic collections were reviewed. They underwent 26 thoracoscopies to evacuate undrained blood with or without infection. RESULTS: In 19 patients (76%), the collections were evacuated thoracoscopically. In 4 patients the procedure was converted to an open thoracotomy, and 2 patients required additional procedures to drain these collections. Failure of thoracoscopy correlated with the time between injury and operation and the type of collection, but not with the mechanism of injury. When thoracoscopy was performed in less than 7 days after admission, no cases of empyema were noted at operation. CONCLUSIONS: Videothoracoscopy is an accurate, safe, and reliable operative therapy to evacuate retained thoracic collections. In 90% of the patients in whom the procedure was completed, good results were obtained, reducing hospital stay and possible complications. Videothoracoscopy should be the initial treatment in trauma patients with retained thoracic collections and should be used earlier and more frequently in these patients.

Nonoperative management of bilateral shattered kidneys from blunt trauma.

Bilateral shattered kidneys secondary to blunt abdominal trauma has not, to our knowledge, been reported. In the case reported herein, severe pulmonary, myocardial, and orthopedic injuries necessitated nonoperative management of this peculiar injury. The patient recovered without sequelae related to the renal injury.

Thoracoscopy in the management of posttraumatic persistent pneumothorax.

BACKGROUND: Persistent posttraumatic pneumothorax (PPP) is an uncommon complication of traumatic injuries of the chest, usually managed with suction drainage and involving prolonged hospital stays. This study was conducted to assess the advantages of using video-assisted thoracoscopic surgery (VATS) in the management of patients with PPP. STUDY DESIGN: Eleven patients with PPP underwent VATS for diagnosis and for definitive treatment. RESULTS: Before VATS was done, all patients had undergone multiple attempts to resolve the PPP; the hospital stay before VATS was 10 days (range, 4-14 days). In 10 patients, the cause of the PPP was identified and a segmental stapled resection was performed, with complete success in resolving the air leak and obtaining pleural synthesis. In another patient, the source of the air leak was not identified and a thoracoscopically assisted chemical pleurodesis was performed, with immediate cessation of the air leak. All chest tubes were removed within 48 hours of the procedure; 9 patients were discharged within 72 hours of VATS. Preoperative computed tomography of the chest was useful in 2 patients, but bronchoscopy did not disclose any major airway injury. CONCLUSIONS: Videothoracoscopy is an accurate, safe, and reliable alternative to an open thoracotomy in the management of patients with PPP. In the patients in whom the procedure was completed, excellent results were obtained and the hospital stay was reduced. We believe that VATS should be used earlier and more frequently after failure of conservative management in such patients.