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Biomedical subjects

S R Shackford

Publications and source records attributed to S R Shackford.

At least 73 records · Page 4Linked to original sources

The effect of hypertonic resuscitation on pial arteriolar tone after brain injury and shock.

Acute brain injury followed by hemorrhagic shock (HEM) causes prohibitive mortality in trauma patients because these combined events lead to low cerebral blood flow (CBF) and cerebral oxygen delivery (co2del). Proper treatment therefore requires rapid correction of cerebral perfusion deficits. Previous studies have shown that hypertonic crystalloid resuscitation significantly improves CBF and co2del in a model of brain injury and HEM when compared to lactated Ringer's (LR) solution. The mechanism or mechanisms for this advantage, however, are not well understood. We hypothesized that hypertonic fluid resuscitation would reduce pial arteriolar tone after brain injury and HEM resulting in an increase in CBF when compared to LR resuscitation. We measured cerebral and systemic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock over a 5-hour period. Swine were randomized to receive either hypertonic sodium lactate (HSL) or LR fluid resuscitation. The HSL resuscitation produced a significant and sustained elevation in cerebral perfusion pressure and pial arteriole diameter (p < 0.05), and a sustained elevation in CBF after brain injury and HEM when compared with LR. These data suggest that hypertonic fluid resuscitation following brain injury and HEM improves CBF, at least in part, by causing vasodilation of cerebral resistance vessels.

Animals↗

Prophylactic vena cava filter insertion in patients with traumatic spinal cord injury: preliminary results.

Pulmonary embolism (PE) is a devastating complication in patients with traumatic spinal cord injury (SCI). Prophylactic measures such as venous compression hose or low-dose heparin are only partially protective in reducing the risk of venous thromboembolism and are contraindicated in some patients. Because of extended perturbations in fibrinolytic activity, catecholamine effects on platelet aggregation, increased activity of complement and acute phase reactants, abnormally high factor VIII concentrations, and persistent venous stasis with ongoing endothelial damage, the patient with an SCI remains at prolonged risk for venous thromboembolism. A retrospective 5-year review at the Medical Center Hospital of Vermont revealed seven patients with eight documented PEs (three fatal; 2.7%) in 111 SCI patients (6.3%). Six PEs (75%) occurred after discharge from the acute care facility. Median time to PE after injury was 78 days (range, 9-5993). Although comprising only 4% of all trauma admissions, SCI accounted for 31% of all PEs in the total trauma population (2525 patients). Beginning in July 1991, a new prophylaxis protocol was instituted, which included the percutaneous insertion of vena cava filters under local anesthesia in all SCI patients with paraplegia or quadriplegia. Fifteen patients have undergone the insertion of titanium filters. Impedance plethysmography was performed weekly to detect deep venous thrombosis. No complications were associated with vena cava filter insertion. No patients developed deep venous thrombosis during their acute hospitalization (median, 22 d), and no patients have developed PE after filter insertion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Death in the operating room: an analysis of a multi-center experience.

To characterize causes of death in the operating room (OR) following major trauma, a retrospective review of admissions to eight academic trauma centers was conducted to define the etiology of death and challenges for improvement in outcome. Five hundred thirty seven OR deaths of 72,151 admissions were reviewed for mechanism of injury, physiologic findings, resuscitation, patterns of injury, surgical procedures, cause of death, and preventability. Blunt injuries accounted for 61% of all injuries, gunshot wounds (GSW) accounted for 74% of penetrating injuries. Sixty two percent of all patients arrived in shock. Average blood pressure (BP) was 52 mm Hg at the scene and 60 mm Hg on admission, with the period of shock > 10 minutes in 74%. Only 56% were resuscitated to a BP > 90 mm Hg before surgery. Average time to the OR was 30.1 minutes and mean best postresuscitation pH was 7.18. Mean best OR temperature was 32.2 degrees C. Recurrent injury patterns judged as the primary cause of patient death included head/neck injury (16.4%), chest injury (27.4%), and abdominal injury (53.4%). Actual cause of death was bleeding (82%), cerebral herniation (14.5%), and air emboli (2.2%). A different strategy for improved outcome was identified in 54 patients with the following conclusions: (1) delayed transfer to the OR remains a problem with significant BP deterioration during delay, particularly following interfacility transfer; (2) staged injury isolation and repair to allow better resuscitation and warming may lead to improved results; (3) combined thoraco-abdominal injuries, particularly with thoracic aortic disruption, often require a different sequence of management; (4) aggressive evaluation of retroperitoneal hematomas is essential; (5) OR management of severe liver injuries remains a technical challenge with better endpoints for packing needed; and (6) resuscitative thoracotomy applied to OR patients in extremis from exsanguination offers little.

Adult↗

Functional limitation after major trauma: a more sensitive assessment using the Quality of Well-being scale--the trauma recovery pilot project.

Little is known about the degree of disability and quality of life of patients after major trauma. We conducted a prospective study to examine the incidence and predictors of functional limitation (FL). Between January 1, 1990 and March 30, 1990, 61 eligible trauma patients were enrolled in the study (admission GCS score > or = 12, LOS > 24 hours). Functional limitation after trauma was measured at discharge and 3 months after discharge using the Quality of Well-being (QWB) scale, a more sensitive index to the well end of the functioning continuum (range, 0 = death to 1.000 = optimum functioning). Functional limitation was also measured using a standard ADL scale (range, 17 = full function to 41 = maximum dysfunction). Risk factors measured were injury severity, body region, depression (CES-D) scale, and social support. Follow-up was achieved in 42 patients (70%). The mean age was 30 years, 74% were male, 52% white, 41% hispanic, and 3% other. The mean ISS was 15, with 69% blunt injuries and a mean LOS of 12 days. The QWB scores improved between discharge and follow-up; discharge mean = 0.457 (+/- 0.048), follow-up mean = 0.613 (+/- 0.118), but the mean QWB score at follow-up still reflected a significant degree of functional limitation. The mean percentage of change in QWB scores was 34.5% (+/- 25.5%) with a range of -6.34% to 103.8%. The discharge mean FDS was 29 (+/- 6.2) while the follow-up FDS mean was 17 (+/- 3.8), reflecting that most patients at follow-up reported near-perfect ADL functioning.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗

The epidemiology of traumatic death. A population-based analysis.

Despite the proliferation of trauma systems, there are no population-based data describing the epidemiology of traumatic death. To provide these data, we reviewed all trauma deaths occurring in San Diego (California) County during 1 year. There were 625 traumatic deaths during the study (27.3 deaths per 100,000 population per year). Motor vehicle trauma was the most common cause of injury leading to death (N = 344 [55.2%]; 15.0 annual deaths per 100,000 population). Central nervous system injuries were the most common cause of death (48.5%, or 13.2 deaths per 100,000 population per year). Sepsis was responsible for only 2.5% of the overall mortality. Based on life-table data, traumatic death resulted in an annual loss of 1091 years of life per 100,000 and an annual loss of 492 years of productivity per 100,000. Injury continues to account for an enormous loss of life despite improvements in survival wrought by trauma systems.

Accidents, Traffic↗

The effect of hypotension and hypoxia on children with severe head injuries.

Survival of children (< 17 years) with severe head injuries (Glascow Coma Scale [GCS] score < 8) has been shown to be better than that of adults. The addition of hypotension (HT) or hypoxia (H) has a deleterious effect on outcome in adults but no information is currently available about their effects in children. Over a 5-year period, 58 children with GCS scores < 8 were admitted and prospectively evaluated at this institution. Patients were divided into two groups on the basis of systolic blood pressure (SBP) and arterial blood gasses. Patients exhibiting HT, defined as a SBP < 90 mm Hg, and patients demonstrating H with a PaO2 < 60 mm Hg were compared with normoxic, normotensive children. Survival was increased fourfold in patients with neither H nor HT as compared with children with either H or HT (P < .001). To validate these observations we reviewed the data from the National Pediatric Trauma Registry for similar patients and included our cohort in the analysis. In total, 509 children had sufficient data for analysis and were studied. Hypoxia alone was not associated with increased mortality in normotensive patients (P = .34). Hypotension significantly increased mortality in these children even without concomitant H (P < .00001). If both HT and H were found together, mortality was only slightly increased over those children with HT alone (P = .056). These data confirm that HT with or without H causes significantly increased mortality in head-injured children to those levels normally found in adults (P = .9), alleviating any age-related protective mechanisms normally afforded.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The epidemiology of injury in a rural state: 5,322 cases over 6 years.

Presently, descriptions of rural trauma are complications of national sample statistics and local data from states projected to rural areas. This study reviews all hospital discharges (36,866) for children (aged 0 to 18 years) from January 1985 through December 1990 in an entirely rural state. Fourteen percent of admissions (5,322) were due to traumatic injury and 63% of these occurred in boys. Injury rates were age dependent with children 15 to 18 years experiencing an incidence of 110/10,000; 10 to 14 years 55/10,000; 5 to 9 years 39/10,000; 1 to 4 years 35/10,000; and < 1 year 39.5/10,000. Mean age for the entire population was 11.4 +/- 5.7 years. Thirty-five percent of children had more than one major site of injury. Sixty-three percent of admissions were for blunt trauma and only 4.8% were penetrating. The remainder were due to burns, hanging, ingestion, and other toxic agents. Falls constituted the most prevalent cause of injury in this population occurring in 25.9%, motor vehicle accidents 22.9%, struck by an object 9.6%, suicide attempts 8.5%, poisoning 4.7%, fire 1.2%, drowning 0.7%, and farm machinery 0.3%. The vast majority of motor vehicle accidents involved the child as an operator or occupant of the vehicle. Less than 10% involved a pedestrian being struck and less than 5% involved a child being struck while on a bicycle. Less than 6% of all injuries involved a bicycle. Child maltreatment was recorded in less than 2% of this population. Only 3.3% of injured children required transfer to another acute care facility (1/3 because of a motor vehicle accident and 1/4 because of a fall).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

The effect of secondary insults on mortality and long-term disability after severe head injury in a rural region without a trauma system.

Outcome after head injury appears to be adversely affected by secondary insults such as hypoxia or hypotension. Previous work examining the influence of these secondary insults on outcome has originated from urban environments with organized systems of trauma care. We hypothesized that secondary insults would be more frequent and that outcome of severe head injury would be worse in a rural region without a trauma system. To validate these hypotheses we retrospectively reviewed the course and outcome of all patients admitted to the Medical Center Hospital of Vermont with severe head injuries between 1980 and 1985. A cohort of 170 patients was assigned to one of two groups: group I had neither hypotension nor hypoxia at the time of admission; group II had either hypotension or hypoxia at the time of admission. The groups were similar in terms of demographics, incidence of mass lesions, frequency of craniotomy, and incidence of intracranial hypertension. Only 23% of group II patients made a good recovery compared with 56% of group I patients (p < 0.01). The mortality rate of group II patients was twice that of group I patients (66% vs. 33%; p < 0.01). When compared with data provided by the National Trauma Coma Data Bank from urban areas with trauma systems, there was no difference in outcome of patients similarly grouped according to the presence or absence of secondary insults between Vermont's rural cohort and the urban cohort. We conclude that hypotension and hypoxia adversely effect the outcome of severe head injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

In-house board-certified surgeons improve outcome for severely injured patients: a comparison of two university centers.

The benefit derived from in-house board-certified attending surgeons (IHBCS) staffing trauma centers has recently been questioned. We compared the outcomes and provider-related complications of patients with severe injuries who were treated at two university trauma centers, one with IHBCS, and one with PGY-4 or PGY-5 residents in house (RIH). The RIH center had a significantly longer resuscitation time (160 vs. 58.8 minutes; p < 0.01). Except in cases of vascular injury, the odds ratio of dying at the RIH institution was significantly greater in all groups when the variables of transport time, Revised Trauma Score, and ISS were controlled. Errors in judgment were significantly more likely to have been made at the RIH institution in all groups. It is concluded that the management and ultimate outcome are significantly improved when IHBCS are involved with the resuscitation and early care of specific cohorts of severely injured patients.

Adult↗

The association of leukocytes with secondary brain injury.

Shock increases mortality from brain injuries, but the mechanism is poorly understood. We hypothesized that brain injury followed by shock and resuscitation leads to a secondary reperfusion injury mediated in part by polymorphonuclear leukocytes (PMNs). To validate this hypothesis, we studied cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral blood flow (CBF), cortical water content (CWC), and hemodynamic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock. Cerebral PMN accumulation (CPMN) in the injured and uninjured hemispheres was determined histologically from the total PMNs in five high-power fields (400x). Twenty-nine mature swine were randomized to four groups. Group 1, the control group, was instrumented only. Group 2 animals had a brain injury alone and were studied for 24 hours. Group 3 animals had a brain injury and hemorrhagic shock. Group 4 animals had hemorrhagic shock alone. Brain injury followed by shock caused a significantly greater ICP and a significantly lower CBF than brain injury or shock alone. There was no significant difference in CPP between groups after resuscitation. The CWC of the lesioned area was similar in both brain-injured groups but was significantly increased when compared with the controls and the shock-only group. The CWC of the nonlesioned hemisphere was higher in group 3 than in group 2. The CPMN in both hemispheres in group 3 was significantly greater than in either group 2 or group 4. There was a significant positive correlation between CPMN and both ICP and CWC, and a significant negative correlation between CPMN and CBF. These data suggest an association between CPMN accumulation and secondary brain injury.

Animals↗

Effect of lesion volume on cerebral hemodynamics after focal brain injury and shock.

Cerebral blood flow (CBF) varies unpredictably in patients after head injury and hemorrhagic shock. Proper treatment requires knowledge of ischemic versus hyperemic flow. The degree to which the size or severity of the injury may contribute to CBF abnormalities is unknown. We hypothesized that lesion size is a determinant of postinjury CBF. We measured cerebral and systemic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock over a 5-hour period. Swine were randomized to receive either a large or small lesion followed by hemorrhage. In the small lesion group traumatic brain injury, followed by shock and resuscitation, produced a significant and sustained elevation in bihemispheric regional CBF and cerebral oxygen delivery that was significantly greater than that observed in either the large lesion group or the controls (p < 0.05). There were no significant differences between the experimental groups in volume of hemorrhage, intracranial pressure, cerebral perfusion pressure, arterial oxygen content, or PaCO2. These data suggest that the volume of injured tissue may determine post-resuscitation CBF, and that interventions to reduce cerebral blood volume (i.e., hyperventilation) may not be universally applicable in all head injured patients.

Animals↗

Prophylactic vena cava filter insertion in severely injured trauma patients: indications and preliminary results.

Pulmonary embolism (PE) remains a significant problem in trauma patients. A 5-year review at this institution revealed 25 PEs (seven fatal) in 2525 admitted trauma patients (1% incidence). Three groups of high-risk patients were identified: (1) those with severe head injury and coma; (2) those with spinal cord injuries with neurologic deficit; and (3) those with pelvic and long bone fractures. The relative risk of PE in these high-risk patients was 21 to 54 times that of the general trauma population. Beginning in July 1991, as prophylaxis against PE, vena cava filters (VCF) were inserted in patients whose injuries placed them in a high-risk group. Thirty-four patients had VCFs inserted percutaneously in the radiology suite without complications. On follow-up examination, 17.6% developed documented lower extremity deep vein thrombosis. There were no PEs. Overall, the incidence of PE in the general trauma population was significantly decreased from 1% to 0.25% (p < 0.05; chi 2). We conclude that insertion of VCFs in high-risk trauma patients is safe and efficacious in decreasing the incidence of PE.

Adult↗

Hemorrhagic hypotension after brain injury causes an early and sustained reduction in cerebral oxygen delivery despite normalization of systemic oxygen delivery.

Morbidity and mortality are doubled when hemorrhagic hypotension (HEM) accompanies a traumatic brain injury (TBI). Hemorrhagic hypotension initiates a "secondary" injury (SI) that has been attributed to ischemia, but this has not been confirmed in the laboratory. All previous studies have been of relatively short duration (less than 6 hours), allowing insufficient time to study the pathophysiology of SI, since maximal intracranial pressure (ICP) elevations may occur 16 to 20 hours after injury. We hypothesized that HEM combined with TBI would reduce cerebral oxygen delivery (cO2del) and cerebral metabolic rate for oxygen (cMRO2) to a greater degree than would occur with TBI alone. In a porcine model of TBI and HEM we recorded systemic oxygen delivery (sO2del), ICP, cerebral blood flow (CBF), cO2del, cMRO2, brain oxygen extraction ratio (cO2ER), and cortical water content (CWC) over a 24-hour study period. Controls (n = 7) were instrumented only, group 1 (n = 14) received a focal cryogenic lesion only, group 2 (n = 21) received a cryogenic lesion plus hemorrhage to 50 mm Hg for 45 minutes. Animals were resuscitated with crystalloid solutions; shed blood in group 2 animals was returned after one hour. Hemorrhagic hypotension following TBI produced a significant and sustained reduction in cO2del associated with a lower cMRO2 and cO2ER, and higher ICP and CWC, than seen with lesion alone. This occurred despite adequate early restoration of sO2del. This confirms that cerebral ischemia is ongoing despite restoration of systemic hemodynamics.

Animals↗

Focal brain injury results in severe cerebral ischemia despite maintenance of cerebral perfusion pressure.

Severe head injury often causes an increase in intracranial pressure (ICP) and decreases in cerebral blood flow (CBF) and cerebral oxygen delivery (CO2del). To determine if this reduction in CBF and CO2del would produce cerebral ischemia and if this reduction would be abrogated by maintaining global cerebral perfusion pressure (CPP), we studied CPP, ICP, CBF, CO2del, cerebral oxygen extraction ratio (CO2ER), and cortical water content (CWC) in a porcine model of focal cryogenic brain injury. Fifteen mature swine were randomized to two groups. The experimental group (n = 7) had a brain lesion and was studied for 24 hours. The control group (n = 8) was instrumented only. Cryogenic injury significantly increased ICP and decreased CBF and CO2del compared with controls. There were no significant differences in CPP between the groups for the entire experiment, and the CPP was well above the ischemic threshold. The CO2ER significantly increased in the first three hours after brain injury. However, CO2ER in experimental animals tended to decrease 12 hours after brain injury and was not significantly different from that in controls. Cryogenic injury significantly increased the CWC in the lesioned hemisphere. These data indicate that focal brain injury results in persistent ischemia despite the normalization of CPP, suggesting that a significant increase in cerebral vascular resistance (CVR) occurs after brain injury. We conclude that in addition to maintenance of CPP, intervention to reduce CVR may be important in the management of brain injury.

Animals↗