Scott R. Petersen

Delayed diagnosis of cervical spine injuries

Over a 32-month period, the cases of all patients with multiple injuries on whom cervical spine roentgenograms (CSRs) were obtained during blunt trauma evaluation in a trauma center were reviewed to determine the incidence, outcome, and clinical consequence of delayed diagnosis of cervical spine injuries. A total of 1,331 patients had CSRs following blunt injury. Sixty-one (4.6%) of the patients had documented cervical fractures or dislocations. The patients were seriously injured (mean Trauma Score, 12; mean Glasgow Coma Scale score, 11; and mean Injury Severity Score, 30.3). Eleven of the patients died in the trauma room; 9 with fatal atlantoaxial dislocation. Of the 50 survivors (81.9%), neurologic deficits were present in 15 (30%), and 8 of those had complete spinal cord injuries. The diagnosis of the cervical spine injury was made during the initial evaluation in 56 of the 61 patients (91.8%). Five patients had delayed recognition of their cervical spine injury (2-21 days). The reason for the delay was incomplete CSRs in all patients, despite multiple views (up to 13). The missed injuries occurred in patients in whom complete visualization of the spine was most difficult (i.e., severe degenerative arthritis of the cervical spine in two patients; previous cervical fractures in one patient; instability during resuscitation in one patient). Radiologic misinterpretation occurred in one patient. The diagnosis of cervical spine injury was pursued because of persistent neck pain in two patients, and the development of subtle neurologic findings in three. The neurologic deficits in the three patients resolved.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement of protein synthesis efficiency in parenterally fed trauma victims by adjuvant recombinant human growth hormone.

In the early catabolic phase of severe injury, conventional nutritional support is inadequate to reverse negative nitrogen balance and an anabolic stimulus may be beneficial. The utilization efficiency of body energy sources after injury could be improved by adjuvant recombinant human growth hormone (rhGH) therapy. We measured the protein kinetic response to exogenous rhGH in trauma patients fed parenterally (TPN). Severely injured (mean ISS, 31 +/- 2), highly catabolic (mean nitrogen loss, 19 +/- 2 g/day), and hypermetabolic (mean BEE/REE, 1.41 +/- 0.05), adult (mean age, 46 +/- 5 years), multiple trauma victims (n = 20, 17 men/3 women) were investigated. Rates of whole-body protein kinetics (turnover [WBPT], synthesis [WBPS], breakdown [WBPB], and protein synthesis efficiency [PSE]--the fraction of nitrogen turnover utilized for protein synthesis) were measured using a primed-constant infusion of 18N glycine 48 to 60 hours after injury when the patients were receiving only maintenance fluids without calories or nitrogen. The patients were then fed glucose-based TPN (1.1 x REE; 250 mg N/kg/day) and randomized to receive or not to receive rhGH. Group H (n = 10) received daily rhGH (0.15 mg/kg/day, Somatropin, Genentech, Inc.) intramuscularly at 8 am and group C (n = 10) received only the vehicle of infusion. Protein kinetic measurements were repeated at the end of 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvant recombinant human growth hormone normalizes plasma amino acids in parenterally fed trauma patients.

BACKGROUND The addition of an anabolic stimulant during intensive nutrition therapy in trauma patients seems to be a reasonable adjuvant for minimizing muscle-mass erosion. The plasma free amino acid pattern is the mirror of the net amino acid metabolism, and we have measured the progressive changes resulting from recombinant human growth hormone therapy in trauma victims during nutritional repletion in the early catabolic flow phase of injury. METHODS In 20 severely injured (injury severity scale = 31 +/- 2), highly catabolic, and hypermetabolic adult multiple-trauma patients, we have measured the fasting (day 0) plasma amino acid levels (48 to 60 hours after injury before starting the nutrition therapy) and their progressive changes during 7 days of IV nutrition support (total parenteral nutrition, 1.1 x resting energy expenditure calories, 250 mg of nitrogen per kilogram per day) with or without adjuvant recombinant human growth hormone. Group H (n = 10) randomly received daily recombinant human growth hormone (0.15 mg of Somatropin per kilogram per day) and Group C (n = 10) received the vehicle of infusion. RESULTS Hypoaminoacidemia of trauma is normalized by infusion of recombinant human growth hormone, which indicates its anabolic nature, and this is confirmed in the cumulative nitrogen balance (-281 +/- 139 mg of nitrogen per kilogram per 7 days compared with -809 +/- 151 mg of nitrogen per kilogram per 7 days without recombinant human growth hormone; p < or = .005). This improved nitrogen retention is also reflected in the significantly low blood urea nitrogen levels in the recombinant human growth hormone group, which represents the efficient utilization of the infused amino acids for synthesis of proteins. Elevated plasma insulin-like growth factor-1 levels in Group H compared with those in Group C may also account for this altered amino acid metabolism. CONCLUSIONS Recombinant human growth hormone treatment in combination with conventional total parenteral nutrition in the immediate posttraumatic period improved nitrogen metabolism and normalized the plasma free amino acid levels.

Duodenal trauma: experience of a trauma center.

In the past decade 93 patients with duodenal injury were treated at a trauma center. By chart review, the age, sex, mechanism of injury, time to initial exploration (and the reason for delay), laboratory results, associated injury, extent of duodenal injury, operative repair, use of drains and tube decompression, morbidity, and cause of death were tabulated in order to improve management of these injuries. Of 87 patients surviving until the time of operative repair 73% required no repair (four) or primary closure (59). The remainder had either resection with primary anastomosis (ten), diverticulization (12), or pancreaticoduodenectomy (two). All patients with penetrating trauma were immediately explored. Patients with blunt trauma were explored on the basis of the judgment of house staff and faculty. Overall mortality was 18%. Significant morbidity occurred in 49% of survivors. This urban experience was heavily weighted toward penetrating injury. In this group early death usually resulted from associated vascular injuries. Blunt duodenal injury was less frequently associated with immediate exsanguination. Mortality associated with blunt duodenal injury was usually the result of delayed diagnosis. In blunt duodenal trauma peritoneal lavage is not diagnostic and may often be misleading; in this series 50% of lavages were false negatives. Blunt duodenal trauma, particularly when combined with pancreatic injury or delayed repair, was a lethal combination. A high index of suspicion and aggressive diagnostic evaluation (CT contrast study/amylase) in the emergency department is required in equivocal cases to avoid morbidity and mortality.

Naturally occurring hypothermia is more advantageous than fever in severe forms of lipopolysaccharide- and Escherichia coli-induced systemic inflammation.

The natural switch from fever to hypothermia observed in the most severe cases of systemic inflammation is a phenomenon that continues to puzzle clinicians and scientists. The present study was the first to evaluate in direct experiments how the development of hypothermia vs. fever during severe forms of systemic inflammation impacts the pathophysiology of this malady and mortality rates in rats. Following administration of bacterial lipopolysaccharide (LPS; 5 or 18 mg/kg) or of a clinical Escherichia coli isolate (5 × 10(9) or 1 × 10(10) CFU/kg), hypothermia developed in rats exposed to a mildly cool environment, but not in rats exposed to a warm environment; only fever was revealed in the warm environment. Development of hypothermia instead of fever suppressed endotoxemia in E. coli-infected rats, but not in LPS-injected rats. The infiltration of the lungs by neutrophils was similarly suppressed in E. coli-infected rats of the hypothermic group. These potentially beneficial effects came with costs, as hypothermia increased bacterial burden in the liver. Furthermore, the hypotensive responses to LPS or E. coli were exaggerated in rats of the hypothermic group. This exaggeration, however, occurred independently of changes in inflammatory cytokines and prostaglandins. Despite possible costs, development of hypothermia lessened abdominal organ dysfunction and reduced overall mortality rates in both the E. coli and LPS models. By demonstrating that naturally occurring hypothermia is more advantageous than fever in severe forms of aseptic (LPS-induced) or septic (E. coli-induced) systemic inflammation, this study provides new grounds for the management of this deadly condition.

Septic phlebitis: A neglected disease

A review of 100 patients with peripheral septic phlebitis revealed that 54 per cent of the cases were due to intravenous catheters and 46 per cent were secondary to drug abuse. Eighty per cent of the involved veins were in the arm or neck. Pain was the most common symptom (83 per cent), with erythema and edema the most common physical signs (63 per cent). Eighty per cent of the causative organisms were gram-positive bacteria, usually Staphylococcus aureus (41 per cent) or Group A streptococcus (20 per cent). Complications were more common if septic phlebitis was due to intravenous therapy than drug abuse. No deaths were directly attributed to septic phlebitis. However, hospital stay after development of septic phlebitis was 14 days with a 56 per cent complication rate. The initial treatment of septic phlebitis should include prompt removal of the intravenous device, antibiotics, heat, and elevation. Because serious complications occur in a significant number of patients, operative excision of the involved vein should be performed if clinical deterioration occurs or if septicemia persists after 24 hours despite conservative therapy.

Pulsatile nature of growth hormone levels in critically ill trauma victims

BACKGROUND Circulating growth hormone (GH) levels in normal persons fluctuate widely because of pulsatile GH secretion. It is not known whether this pulsatile nature and rhythmicity exist in severe injury. These data become necessary to decide the timing of supplementary GH administration for its optimal utilization. The purpose of this study was to investigate the GH circadian variation with respect to that of insulin-like growth factor-1 (IGF-1), insulin, C-peptide, and cortisol in the early flow phase of injury. METHODS Plasma GH, IGF-1, insulin, C-peptide, and cortisol levels were measured at 1-hour intervals during 24 hours (8 AM to 8 AM) in 10 severely injured adults with multiple trauma during the early catabolic flow phase 24 to 48 hours after injury, when patients received maintenance fluids without calories or nitrogen. RESULTS The 24-hour integrated GH concentration is not different from either 12-hour mean diurnal or 12-hour mean nocturnal or mean 8 AM GH concentration. Pulsatile GH bursts persist in injured patients during both day and night. Pulsatile bursts do not exist for IGF-1, insulin, and C-peptide. The plasma levels of cortisol show time-dependent daily maximum and minimum levels. CONCLUSIONS Pulsatile GH bursts persist in injured patients but less frequently than seen in normal persons. The time of bolus administration of GH to augment the anabolic GH action in patients with trauma does not matter; however, for convenience morning administration may be preferable for patients in the intensive care unit.

Enteral nutritional support and wound excision and closure do not prevent postburn hypermetabolism as measured by continuous metabolic monitoring.

BACKGROUND Estimation of nutritional needs in burn patients is difficult. In 24 severely burned patients, we measured CO2 production and O2 consumption continuously during their period of mechanical ventilation. METHODS Patients with extensive burns were placed on a continuous metabolic monitor (CMM) (Puritan Bennett Co., Kingwood, TX), and metabolic expenditure was recorded each 24 hours. High protein enteral feedings were started within several hours of admission, and administration rates were adjusted to meet daily caloric demands as determined by the CMM. Full-thickness wounds were excised as early as patient condition permitted, and wounds were closed with autograft, allograft, or TransCyte (Advanced Tissue Sciences Inc., La Jolla, CA). Daily 24-hour caloric needs as measured by CMM were compared with baseline caloric needs predicted by the Harris-Benedict equation and also compared with actual daily caloric intake. Patients were removed from study when they were off continuous mechanical ventilation. RESULTS A total of 24 patients were studied, with a mean age of 46 years and a 44% total body burn size (partial- and full-thickness). All full-thickness burns were completely excised by a mean of 6.5 days postburn. Mean daily energy expenditures remained elevated through the duration of the study period (42 days), with a mean elevation of 184.9% of baseline as predicted by Harris-Benedict equation. Patients received enteral feedings, which met 99.4% of actual caloric needs as predicted by CMM during the study period. CONCLUSION Continuous metabolic monitoring demonstrates that early wound excision and wound closure, coupled with aggressive enteral nutritional support with high protein formulas, do not prevent the marked hypermetabolism that accompanies thermal injury.

Reprioritization of liver protein synthesis resulting from recombinant human growth hormone supplementation in parenterally fed trauma patients: the effect of growth hormone on the acute-phase response.

BACKGROUND One of the major components of the metabolic response to severe trauma is the alteration in concentrations of a large number of plasma proteins referred to as acute-phase proteins (APP). The principle mediators of these liver-synthesized APP are mainly the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). METHODS We have measured the plasma levels of IL-6, TNF alpha, and 20 APP in 24 adult, severely injured, hypermetabolic and highly catabolic patients with multiple injuries within 48-60 hours after injury, when they were receiving maintenance fluids without calories or nitrogen, and subsequently during 7 days of total parenteral nutrition with (n = 12) or without (n = 12) recombinant human growth hormone supplementation (rhGH, 0.15 mg/kg/d). RESULTS Baseline positive APP due to severe trauma include C-reactive protein (CRP), alpha-1 antichymotrypsin, alpha-1 acid glycoprotein, alpha-1 antitrypsin, fibronectin, and factor B. Negative APP include IgG, IgM, complement-3, prealbumin, transferrin, ceruloplasmin, and albumin. Except for CRP, alpha-1 antichymotrypsin, and albumin, all the APP levels increase during 7 days of nutritional support. Plasma levels of cytokines IL-6 and TNF-alpha, although initially markedly increased after injury, decrease with parenteral refeeding. There is a linear correlation between CRP and IL-6 levels and also between the transport proteins prealbumin and transferrin. Trauma-induced increases in CRP and IL-6 levels decreased with nutrition alone, but did not change with rhGH supplementation. An immunosuppressed state of injury is evident from the decreased immunoglobulin levels (IgG, IgM, IgA) in the trauma patients. Total parenteral nutrition alone increases the immunoglobulin levels to normal. However, with adjuvant rhGH, only IgA levels are normalized. CONCLUSIONS Adjuvant rhGH therapy does not attenuate the reprioritization of acute liver protein synthesis and results in only limited restoration of host defenses. The clinical implications of these findings await further study.

Management of injuries to the porta hepatis.

The management of injuries to the porta hepatis is challenging and controversial. Although definitive, anatomic reconstruction of injured ductal or vascular structures is optimal, porta hepatis injuries are universally accompanied by injuries to other organs (3.6 in this series), which often precludes initial repair. Moreover, frequent injury to the inferior vena cava, aorta, or other major blood vessels in addition to the structures of the porta hepatis results in these injuries being treated in conjunction with exsanguinating hemorrhage. For that reason, control of hemorrhage is the initial management priority, with the initial operation requiring expeditious, if less than anatomically exact, operations. Eighteen of 31 patients survived porta hepatis injury. Hepatic artery injuries were treated by ligation. Complex injuries to bile ducts frequently required enteric-ductal anastomoses as secondary procedures. Of 29 patients with portal vein injuries, six were treated by ligation, 22 by lateral repair, and one with splenic vein interposition graft. As in earlier reports, the structure of the porta hepatis associated with the highest morbidity and mortality rates when injured was the portal vein.