Planned ventral hernia following damage control laparotomy in trauma: an added year of recovery but equal long-term outcome.

PURPOSE: Significantly injured trauma patients commonly require damage control laparotomy (DCL). These patients undergo either primary fascial closure during the index hospitalization or are discharged with a planned ventral hernia. Hospital and long-term outcomes of these patients have not been extensively studied. METHODS: Patients who underwent DCL for trauma from 2003 to 2012 at a regional Level I trauma center were identified and a comparison was made between those who had primary fascial closure and planned ventral hernia. RESULTS: DCL was performed in 154 patients, 47% of whom sustained penetrating injuries. The mean age and injury severity score (ISS) were 40 and 25, respectively. Hospital mortality was 19%. Primary fascial closure was performed in 115 (75%) of those undergoing DCL during the index hospitalization. Of these, 11 (9%) had reopening of the fascia. Of the surviving patients, 22 (19%) never had primary fascial closure and were discharged with a planned ventral hernia. Patients with primary fascial closure and those with planned ventral hernia were similar in age, gender, ISS, and mechanism. Those with planned ventral hernias underwent more subsequent laparotomies (3.0 vs. 1.3, p < 0.001), and had more enteric fistulas (18.2 vs. 4.3%, p = 0.041) and intra-abdominal infections (46 vs. 15%, p = 0.007), and had a greater number of hospital days (38 vs. 25, p = 0.007) during the index hospitalization. Sixteen (73%) patients with a planned ventral hernia had definitive reconstruction (mean days = 266). Once definitive abdominal wall closure was achieved, the two groups achieved similar rates of return to work and usual activity (71 vs. 70%, p = NS). CONCLUSIONS: Following DCL for trauma, patients with a planned ventral hernia have definitive reconstruction nearly 9 months after the initial injury. Once definitive abdominal wall closure has been achieved; patients with primary fascial closure and those with planned ventral hernia have similar rates of return to usual activity.

Carotid arteriography impacts carotid stenosis management.

Recent literature advocates carotid endarterectomy on duplex alone. The authors hypothesized that carotid angiography adds information that alters clinical management in a substantial number of patients compared to the use of carotid duplex examination alone. The records of 182 consecutive patients who underwent carotid artery duplex and subsequent carotid/cerebral angiography for suspected carotid artery stenosis between January 1998 and April 1999 were reviewed retrospectively. Carotid artery duplex examinations were stratified based on stenosis: < or =39%, 40% to 59%, 60% to 79% (moderate), 80% to 99% (severe), 100%. Carotid stenosis on angiograms was determined by NASCET criteria. New information found at angiography included vertebral, subclavian, or arch atherosclerosis, intracranial pathosis, or a change in duplex stenosis category to a degree of stenosis not requiring surgery. Clinical importance was attributed to angiograms that altered the patients' management plan. Angiography provided additional information in 53% (97/182) of patients. Vertebral disease was found in 25.1%, subclavian disease in 16.4%, intracranial disease in 15.3%, aortic arch disease in 3.3%. Patient treatment was altered in 30% (55/182). Angiographic findings downgraded the stenosis to medical therapy in 20.9% (38/182). The surgical plan was influenced in 5.5% (10/182). Nine intracranial aneurysms were discovered. Carotid angiography was essential for vascular bypass surgery planning in 3.3% (6/182). Angioplasty was performed in 2.2% (4/182). The accurate determination of stenosis is critical in determining optimal treatment of patients with carotid artery stenosis. Routine carotid angiography remains valuable in the clinical treatment of these patients.

The "July phenomenon" and the care of the severely injured patient: fact or fiction?

BACKGROUND: The "July phenomenon," a common belief in medical academia, refers to purported errors, inefficiency, and negative outcomes during the summertime transition of the house staff. We hypothesized that care in a trauma service is consistent throughout the year and that the July phenomenon therefore is a myth. METHODS: The records of adults admitted to a trauma service between July 1994 and September 1999 were evaluated. The care of and outcomes for patients admitted in July and August were compared with those of patients admitted in April and May. RESULTS: Nine hundred seventeen patients were evaluated over 5 years. Patients were well matched by the Injury Severity Score, the Glasgow Coma Score, by mechanism, and by survival probability. Patients admitted in the spring were significantly older, by a mean of 5.1 years. Length of stay and intensive care unit stay were similar. Emergency department times were similar, as were resuscitation times, infection rates, and hospital costs. The mortality of patients was similar between the 2 times. CONCLUSIONS: There was no evidence of an increase in negative outcomes early in the academic year compared with the end of the academic year. We believe that a systematic approach to the diagnosis, resuscitation, and treatment of trauma prevented a July phenomenon.

Laparotomy potentiates cytokine release and impairs pulmonary function after hemorrhage and resuscitation in mice.

BACKGROUND: The two-hit theory has emerged as a mechanism to explain the development of organ failure after traumatic injury. We evaluated the effects of exploratory laparotomy (EL) as a second hit on mice after hemorrhage and resuscitation (H/R). Our hypothesis was that mice exposed to prior H/R would demonstrate more evidence of acute lung injury (ALI), as well as an augmented cytokine response, than mice exposed to H/R or EL alone. METHODS: Three groups of mice were examined. Mice undergoing H/R alone were labeled as the H/R group. Mice undergoing sham H/R (cannulation but no hemorrhage), followed 5 days later by EL, were labeled as the EL group; and mice undergoing H/R, followed 5 days later by an EL, were labeled as the H/R + EL, or two-hit, group. Respiratory function was determined by using whole-body plethysmography and lung gas diffusion. Serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were assayed at 1 and 4 hours after the injury stimuli. RESULTS: Evaluation of the change in pulmonary function after 24 hours demonstrated that EL alone induces a significant decrease in pulmonary function, whereas two-hit mice did not exhibit a potentiated response. Alveolar function was significantly degraded in the EL group compared with all other groups (p < 0.0001). TNF-alpha did not change after any injury at any time. However, evaluation of IL-6 levels demonstrated a substantial increase after H/R, EL, and H/R + EL compared with baseline and at 1 hour. Comparison of the three groups at 4 hours did not demonstrate any differences in serum concentrations of IL-6. Histologic evaluation lungs demonstrated that the most severe lung injury was seen in the EL mice. CONCLUSION: It would appear that serum TNF-alpha has little impact on the pathogenesis of ALI after EL, whereas serum IL-6 may be more important. Exploratory laparotomy resulted in a significant change in pulmonary function. Contrary to our initial hypothesis, two-hit mice did not demonstrate more evidence of ALI and, in fact, demonstrated less lung injury than EL mice.

Hemorrhage and resuscitation induce delayed inflammation and pulmonary dysfunction in mice.

BACKGROUND: It is well known that hemorrhagic shock induces inflammatory changes. Our objective was to study the histologic and biochemical changes in the lung and evaluate alterations in respiratory function after hemorrhage and resuscitation (H/R) in mice. METHODS: After 30 min of hemorrhagic shock, mice were resuscitated with shed blood to restore mean arterial blood pressure to baseline. A sham group was anesthetized and instrumented for 30 min, but did not undergo hemorrhage. Myeloperoxidase (MPO) levels were measured and histologic analysis was performed on lung tissue. Pulmonary function was evaluated using whole-body plethysmography (WBP) 1, 3, and 5 days postprocedure. Alveolar function was evaluated by measuring carbon monoxide uptake via gas chromatography 5 days after H/R. RESULTS: Five days after H/R, mice exposed to shock had significantly higher lung MPO levels and showed greater histologic evidence of lung injury. Airway resistance (Penh) in the sham mice was 0.91 +/- 0.06 versus 1.21 +/- 0.09 in the hemorrhage group (P < 0.01). Alveolar function was significantly decreased in the H/R group (70.8 +/- 3.6%) compared with shams (81.6 +/- 1.8%) (P < 0.05). CONCLUSIONS: Hemorrhage and resuscitation cause delayed biochemical, histologic, and physiologic changes in the lung. These were marked by increased lung MPO, increased neutrophils, and decreased alveolar function. The alterations of pulmonary function and structure were most severe 5 days after H/R.

Occult hypoperfusion is associated with increased morbidity in patients undergoing early femur fracture fixation.

BACKGROUND: The presence of persistent occult hypoperfusion (OH) is associated with higher morbidity and mortality rates after trauma. Early femur fracture fixation in trauma patients with multiple injuries is associated with decreased morbidity and mortality. Association of OH and incidence of postoperative complications after intramedullary (IM) fixation in patients with femur fractures was investigated. METHODS: A retrospective study design was used. All patients with femur fractures admitted to the trauma service of a Level I trauma center between January 1, 1995, and August 1, 1998, who were older than 18 years of age and who had IM fracture fixation within 24 hours of admission and serum lactate determinations on admission and at proscribed intervals, were included in the study. Patients with lactic acid levels > or = 2.5 mmol/L were determined to have OH. No patients had clinical signs of shock (hypotension, tachycardia, decreased urine output) on transfer to the operating room. Complete resuscitation was defined as a lactic acid level < 2.5 mmol/L. Patients were divided into two groups based on presence/absence of OH determined from the lactic acid level immediately before surgery. The incidence of all postoperative organ complications was recorded, and complication rates were compared between groups. Total hospital costs were also compared. RESULTS: One hundred seventy-seven patients with femur fractures were admitted to the trauma service during this period. Seventy-nine patients met initial criteria for inclusion in the study. Further review excluded 32 patients. Occult hypoperfusion was present in 20 patients before early IM fixation (group 2). Twenty-seven patients were completely resuscitated before early IM fixation (group 1). Injury Severity Scores were similar in both groups. Group 2 had 35 complications in 20 patients, and group 1 had 11 complications in 27 patients. A significant difference was found in incidence of postoperative complications in group 1 (20%) versus group 2 (50%). Group 2 also had a significantly higher proportion of postoperative infections than group 1 (72% vs. 28%, respectively) and higher total hospital costs ($46,469 vs. $23,139). CONCLUSION: The presence of OH in trauma patients undergoing early IM fixation of a femur fracture is associated with a twofold higher incidence of postoperative complications. Clinical judgment, not surgical dogma, should guide the timing of IM fixation in these patients. Identifying and correcting OH through relatively simple resuscitative measures may be advantageous in reducing morbidity in the patient with multiple injuries.

Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patients.

OBJECTIVE: To investigate the hypothesis that occult hypoperfusion (OH) is associated with infectious episodes in major trauma patients. METHODS: Data were collected prospectively on all adult trauma patients admitted to the Surgical/Trauma Intensive Care Unit from November of 1996 to December of 1998. Treatment was managed by a single physician according to a defined resuscitation protocol directed at correcting OH (lactic acid [LA] > 2.4 mmol/L). RESULTS: Of a total of 381 consecutive patients, 118 never developed OH and 263 patients exhibited OH. Seventeen patients were excluded because their LA never corrected, and they all subsequently died. One hundred seventy-six infectious episodes occurred in 97 of the 364 patients remaining. The infection rate in patients with no elevation of LA was 13.6% (n = 118) compared with 12.7% (n = 110) in patients whose LA corrected by 12 hours, 40.5% (n = 79; p < 0.01 compared with all other groups) in patients whose LA corrected between 12 and 24 hours, and 65.9% (n = 57; p < 0.01 compared with all other groups) in patients who corrected after 24 hours. Among the patients with infections, there were 276 infection sites with 42% of infections involving the lung and 21% involving bacteremia. There was no difference in proportion of infections occurring at each site between groups. The mortality rate of patients who developed infections was 7.9% versus 1.9% in patients without infections (p < 0.05). Of the patients who developed infections, 69.8% versus 25.8% (p < 0.001) did not have their lactate levels normalized within 12 hours of emergency room admission. Logistic regression demonstrated that both the Injury Severity Score and OH > 12 hours were independently predictive of infection. CONCLUSION: A clear increase in infections occurred in patients with OH whose lactate levels did not correct by 12 hours, with an associated increase in length of stay, days in surgical/trauma intensive care unit, hospital charges, and mortality.

A successful multimodality strategy for management of liver injuries.

The treatment of liver injuries involves many strategies ranging from observation to operative intervention and includes numerous options such as angiography, packing, and damage-control procedures. In July 1994 we instituted a protocol for the management of traumatic liver injuries. The main objective of this study was to evaluate the management of liver injuries occurring since the institution of the protocol. Two hundred three consecutive adult patients with liver injuries were evaluated at our Level I trauma center between July 1994 and May 1999. Eighty-eight per cent of the injuries were blunt with a mean Injury Severity Score (ISS) of 24.3 +/- 0.8 and a survival probability (Ps) of 90.0 +/- 1.5 per cent. The overall mortality was 6.4 per cent. A comparison between patients with minor liver injuries and patients with more severe injuries [Abbreviated Injury Score (AIS) <3 vs >3] demonstrated no difference in mortality between the two groups despite a Ps of 93.8 +/- 1.3 per cent in patients with an AIS <3 versus 84.1 +/- 3.3 per cent in patients with an AIS >3. The most common complication in our patient population was posthemorrhagic anemia, which was seen in 10.8 per cent of cases. Severity of injury did not result in a significant difference in the complication rate. Patients who underwent laparotomy had a statistically higher ISS, a lower Ps, and a mortality rate of 11.5 per cent compared with 3.7 per cent (P = 0.03) in patients managed nonoperatively. However, a comparison of patients undergoing laparotomy with those who did not and who had equivalent ISS demonstrated no difference in mortality. Our results demonstrated that a preplanned management strategy was a successful way in which to treat patients with traumatic liver injuries. Although nonoperative management of liver injuries has been common practice a management plan that involves a multimodal surgical strategy is essential.

The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma.

BACKGROUND: The significance of occult hypoperfusion (OH) in the development of respiratory complications (RC), multiple system organ failure (MSOF), and death, and the effect of rapid identification and correction of OH in the severely injured trauma patient was investigated. METHODS: A pilot retrospective study and the analysis of a prospective protocol to correct OH were performed. Pilot study: all trauma patients admitted to our Level I trauma center between February and December of 1995, who survived greater than 48 hours, had an Injury Severity Score greater than or equal to 20, and intensive care unit stays greater than 48 hours were evaluated. Prospective study: patients admitted between January 1, 1996, and April 30, 1997, who survived greater than 24 hours, with Injury Severity Score greater than or equal to 20, and who were hemodynamically stable (systolic blood pressure greater than 100, pulse rate less than 120, and urine output greater than 1 mL/kg per hour) were included. Serum lactic acid (LA) levels were measured at arrival and at proscribed intervals. In the pilot study, initial LA levels were examined in relation to outcome and complications. In the prospective study, patients with two consecutive LA levels greater than 2.5 mmol/L underwent invasive monitoring and vigorous resuscitation to correct their lactic acidosis. RESULTS: Among the 31 patients studied in the pilot study, there were 4 deaths, 6 cases of MSOF, and 13 patients with RC. Lactic acidosis and poor cardiac performance, as evidenced by low cardiac index (CI) with normal filling pressures, were seen in all cases of MSOF and RC, as well as in all deaths. From these results, the prospective study was performed. Eighty-five intensive care unit patients met criteria for inclusion in the study. Six additional patients were excluded because of severe, untreatable intracranial hypertension at admission to the intensive care unit. Fifty-eight of these patients had OH in the first 24 hours. Forty-four patients corrected their OH within 24 hours with vigorous resuscitation. There were no deaths, three cases of MSOF, and 10 cases of RC in those patients who corrected OH within 24 hours. Persistent OH (>24 hours) was seen in 14 patients, despite resuscitative efforts, 43% of whom died. MSOF and RC were present in 36% and 50% of cases, respectively (p<0.05). CONCLUSION: Initial lactic acidosis is associated with lower cardiac performance and higher morbidity and mortality. Persistent OH is associated with higher rates of RC, MSOF, and death after severe trauma. Early identification and aggressive resuscitation aimed at correcting continued elevation in serum lactate improves survival and reduces complications in severely injured trauma patients.

High-frequency oscillatory ventilation can be effective as rescue therapy for refractory acute lung dysfunction.

High-frequency oscillatory ventilation (HFOV) is a technique with limited use in adult patients. The main purpose of this pilot study was to evaluate HFOV on adult trauma patients with refractory lung dysfunction. Refractory lung dysfunction was defined as a PaO2:FiO2 ratio <75 for 1 hour despite maximum support via conventional mechanical ventilation (CMV). Five patients were placed on HFOV after failing CMV between May 1998 and December 1998. The mean PaO2:FiO2 ratio at the time of initiation (52.2+/-4.73) of HFOV increased significantly (P<0.05) by 2 hours (126.8 +21) and was still significantly increased (P<0.01) after 48 hours (181 +26.1) on HFOV. The mean airway pressures (MAPs) and peak pressures were significantly lower (P<0.01) after HFOV. The average MAP of the five patients was 34.6 +1.6 cm H2O at time zero and 25.2 cm H2O after 48 hours of HFOV. The mean peak pressure was 52.4 +3.0 cm H2O at time zero and was 35.8+/-3.01 after termination of HFOV. Survival was 80.0 per cent (four of five patients). In conclusion, all patients improved after initiation of HFOV, and HFOV should be considered in the treatment of patients with acute refractory lung dysfunction.