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.

Postural effects on measurements of tidal volume from body surface displacements.

Tidal volume measurements based on the sum of volume displacements of the rib cage (RC) and abdomen (Ab) are limited in accuracy when changes in posture occur. To elucidate the underlying sources of error, five subjects performed spinal flexion-extension isovolume maneuvers and then performed Konno-Mead isovolume maneuvers at different lung volumes while erect, with the spine fully flexed, and at intermediate degrees of spinal flexion. RC and Ab dimensions were measured with respiratory inductance plethysmograph belts, and spinal flexion was assessed by a pair of magnetometers measuring the xiphi-Ab distance (Xi). RC and Ab volume-motion coefficients (alpha and beta, respectively) were calculated from the slope (-beta/alpha) of the Konno-Mead isovolume lines. We found that 1) spinal flexion with constant lung volume mainly increases the RC dimension, thereby displacing the Konno-Mead isovolume lines, and 2) spinal flexion decreases the -beta/alpha by decreasing beta. The error related to displacement averaged 28.4 +/- 15% of vital capacity, whereas the error related to changes in beta averaged 14 +/- 6% (SD). The systematic relationship of these errors with the degree of spinal flexion provides a mechanism whereby the addition of Xi to RC and Ab displacements significantly (P less than 0.001) improves volume estimates.

Critical pressures required for generation of forced expiratory wheezes.

Flow limitation (FL) has recently been shown to be a necessary condition for the generation of forced expiratory wheezes (FEW) in normal subjects. The present study was designed to investigate whether it is also a sufficient condition. To do so we studied the effects of varying expiratory effort on generation of FEW. Six normal subjects exhaled with varying force into an orifice in line with a high-impedance suction pump. Esophageal (Pes), airway opening, and transpulmonary (Ptp) pressures were measured alongside flow rate, lung volume, and tracheal lung sounds. In each subject a certain critical degree of effort had to be attained before FEW were generated. This effort, measured as Pes at the onset of wheezes, varied among the subjects (range -11 to 45 cmH2O). Similarly, a minimal Ptp had to be reached for FEW to evolve (mean +/- SD -34 +/- 12 cmH2O, range -18 to -50 cmH2O). These critical Pes and Ptp values were significantly higher than those required for FL. It was concluded that, in addition to the requirement for FL, sufficient levels of effort and negative Ptp must exist before FEW can be generated. By analogy to experimental and theoretical results from studies on flow-induced oscillations in self-supporting collapsible tubes, it was further concluded that these pressures are required to induce flattening of the intrathoracic airways downstream from the choke point. It is this configurational change that causes air speed to become equal to or exceed the critical gas velocity needed to induce oscillations in soft-walled tubes.

Pleural pressure increases during inspiration in the zone of apposition of diaphragm to rib cage.

The zone of apposition of diaphragm to rib cage provides a theoretical mechanism that may, in part, contribute to rib cage expansion during inspiration. Increases in intra-abdominal pressure (Pab) that are generated by diaphragmatic contraction are indirectly applied to the inner rib cage wall in the zone of apposition. We explored this mechanism, with the expectation that pleural pressure in this zone (Pap) would increase during inspiration and that local transdiaphragmatic pressure in this zone (Pdiap) must be different from conventionally determined transdiaphragmatic pressure (Pdi) during inspiration. Direct measurements of Pap, as well as measurements of pleural pressure (Ppl) cephalad to the zone of apposition, were made during tidal inspiration, during phrenic stimulation, and during inspiratory efforts in anesthetized dogs. Pab and esophageal pressure (Pes) were measured simultaneously. By measuring Ppl's with cannulas placed through ribs, we found that Pap consistently increased during both maneuvers, whereas Ppl and Pes decreased. Whereas changes in Pdi of up to -19 cmH2O were measured, Pdiap never departed from zero by greater than -4.5 cmH2O. We conclude that there can be marked regional differences in Ppl and Pdi between the zone of apposition and regions cephalad to the zone. Our results support the concept of the zone of apposition as an anatomic region where Pab is transmitted to the interior surface of the lower rib cage.

Forced expiratory wheezes are a manifestation of airway flow limitation.

To study the mechanism of generation of respiratory wheezes we examined the relationships between forced expiratory wheezes (FEW) and flow limitation in the lung. Tracheal lung sounds were measured in six healthy subjects during forced expiration through a flow-limiting valve in series with a high-impedance suction pump. Mouth pressure, esophageal pressure, transpulmonary pressure (Ptp), flow (V), and volume were also measured. For any flow rate, V was constant until the subject became flow limited. The onset of flow limitation was documented by a small change in V and a sudden change in Ptp, which was previously found by Olafsson and Hyatt to correspond to the beginning of the flow plateau of the isovolume pressure-flow curve (J. Clin. Invest. 48: 564-573, 1969). FEW started 107 +/- 45 ml (SD) after the onset of flow limitation. Additional 79 +/- 65 ml were exhaled between the onset of FEW to the final sharp drop in V. The frequency spectra of FEW were the same as those of respiratory wheezes found in obstructive airway diseases. Administration of inhaled bronchodilator (isoproterenol) did not eliminate the FEW, nor did it change their relationship to flow limitation. The sequence of events around the onset of FEW, and the tight correlation with the onset of flow limitation correspond well to recent experimental observations on the onset of flutter in collapsible, thick-walled latex tubes.

Estimates of ventilation from body surface measurements in unrestrained subjects.

To make estimates of ventilation from measurements of body surface movements in unrestrained subjects, we measured changes in linear dimensions and cross-sectional areas of the rib cage (RC) and abdomen (AB) of six healthy unrestrained subjects during a variety of maneuvers. RC and AB anteroposterior diameters and abdominal length in the cephalocaudal axis (axial displacement) were measured with magnetometers, and RC and AB cross-sectional areas were measured with a respiratory inductance plethysmograph. Flow was measured at the mouth with a pneumotachograph and integrated electrically to give volume. Volume and body surface measurements were analyzed by multiple linear regression. Addition of the axial measurements to either the anteroposterior dimensions or cross-sectional areas of RC and AB improved estimates of tidal volume in all subjects (P less than 0.01). With measurements of axial displacement and cross-sectional area of the RC and AB, tidal volume could be reliably estimated to within 20% of actual ventilation. We conclude that measurement of axial displacements improves estimates of ventilation in unrestrained subjects.

Thoracoabdominal blood volume change and its effect on lung and chest wall volumes.

The effects of changing blood volume within the thoracoabdominal cavity (Vtab) have been studied in four male subjects trained in respiratory maneuvers. Subjects were studied lying supine in a pressure plethysmograph with inflatable fracture splints placed around both arms and legs. Changes in Vtab were produced by inflating the splints to 30 cmH2O. Thoracic gas volume (Vtg) measured by Boyle's law, and the change in chest wall volume (delta Vw), measured by anteroposterior magnetometers on rib cage and abdomen, were measured almost simultaneously and at two respiratory system volumes. The quantity of blood moved by splint inflation was estimated for each subject at both respiratory system volumes and varied between 215 and 752 ml. The chest wall increased 64 +/- 11.8% (mean +/- SD) of the increase in Vtab. Thus increases in thoracoabdominal blood volume increase Vw about twice the decrease in Vtg.