Evolution in the management of the complex liver injury at a Level I trauma center.

BACKGROUND: Management of the severe liver injury evolved from mandatory surgical repair to a more selective approach. This paper reviews the changes in management of the severe liver injury at a Level I trauma center. METHODS: We reviewed the records of patients with severe liver injury admitted to a Level I trauma center between January 1984 and December 1995. The patients were divided into two groups, G1 and G2, based on their date of admission before or after January 1991. The two groups were compared for blood products use, management of the liver injury, and outcome. RESULTS: One hundred six patients were compared for age, sex, Acute Physiology and Chronic Health Evaluation II score, Injury Severity Score, abdominal Abbreviated Injury Scale score, and the presence of concomitant injuries. There was no difference in management or outcome of the victims of penetrating injury between G1 and G2 (n = 48). The blunt injury patients in G1 (n = 22) had more liver surgery (p = 0.006), blood transfusion (p = 0.040), intra-abdominal sepsis (6 vs. 0), and higher mortality (p = 0.041) than those in G2 (n = 36). CONCLUSION: Isolated severe blunt liver injury may be managed nonoperatively with better survival and less blood products use.

The efficacy of sequential compression devices in multiple trauma patients with severe head injury.

Thirty-two multiple trauma patients with severe head injury and a Glasgow Coma Scale (GCS) score of 8 or less were prospectively studied to assess the occurrence of deep venous thrombosis (DVT) and pulmonary embolism (PE). All patients required mechanical ventilation. A sequential compression device (SCD) was used in 14 patients and 18 patients received no prophylaxis for thromboembolism. Bilateral lower extremity technetium venoscans and ventilation/perfusion (V/Q) lung scans were performed within 6 days of admission and every week for 1 month or until the patient developed DVT or PE or was discharged from the SICU. Deep venous thrombosis occurred in two patients (6%) at 16 and 28 days following trauma. Twenty-five patients had normal or low probability V/Q scans. Six had high probability V/Q scans confirmed by pulmonary arteriograms (PAGs) at 12.5 +/- 4 days. Clinical signs of PE were absent in all patients with a positive PAG. There were no differences in age, Injury Severity Score (ISS), GCS Score, APACHE II Score, or Trauma Score between the patients who developed DVT or PE and those who did not. A SCD was used in four of the eight patients with DVT or PE. All but one patient with DVT or PE underwent placement of a vena caval filter. Multiple trauma patients with severe head injury (GCS score < or = 8) are at high risk for thromboembolism. The available means of prevention and diagnosis of DVT or PE in multiple trauma patients with severe head injury are not entirely effective.

Management of the trauma patient with pre-existing renal disease.

Chronic renal disease is associated with fluid retention, electrolyte disturbances, anemia, platelet dysfunction, malnutrition, and, often, underlying disease such as diabetes, hypertension, and coronary artery disease. The mortality and morbidity of trauma increases when the victim has pre-existing renal disease. Special attention must be given to fluid resuscitation in these patients because of their limited or absent ability to excrete solutes and fluids. Invasive hemodynamic monitoring is helpful in guiding the resuscitation efforts because urine output and acid-base balance are unreliable markers. Knowledge of pharmacokinetics and pharmacodynamics is necessary in patients with renal disease. Choice of therapy for solute and fluid removal depends on the patient's hemodynamic status, the presence or absence of coagulopathy, and the type of traumatic injury. Renal replacement therapies are recommended for hemodynamically compromised patients.

Changes in hepatocyte NADH fluorescence during prolonged hypoxia.

Deprivation of oxygen reduces oxidative phosphorylation and rapidly causes an increase in cellular NADH which can be monitored by fluorimetry. Previous studies have established that increases in NADH fluorescence accurately reflect the impairment in oxidative phosphorylation which occurs during brief periods of acute hypoxia. However, the potential usefulness of fluorimetry for following longer, clinically relevant periods of ischemia has not been explored. We studied changes in NADH fluorescence in rat hepatocyte suspensions and in isolated-buffer-perfused rat livers during hypoxia (pO2 < 50 mm Hg) for periods as long as 180 min. NADH fluorescence of hepatocyte suspensions consistently increased by about 15% after 13 to 15 min of hypoxia and coincided with a marked decrease in tissue ATP levels. Reoxygenation after 15 or 30 min of hypoxia resulted in recovery of ATP and NADH with minimal loss of viability, as measured by trypan blue exclusion. After 60 to 180 min hypoxia, the initial increase in NADH fluorescence was followed by a progressive, irreversible decline which correlated with decreased cell viability. Similar changes in NADH fluorescence were observed in isolated-perfused rat livers in which NADH fluorescence was monitored at the liver surface with a fiberoptic probe. Hypoxia for 30 min had no effect on NADH fluorescence, but hypoxia for longer periods caused a steady increase in fluorescence after 45-60 min. When hypoxia was prolonged (120 or 180 min), fluorescence peaked after 60-75 min and then declined progressively to levels below baseline. The greatest decrease in fluorescence was seen after 180 min of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

The clinical significance of myocardial contusion.

In an attempt to identify a group of blunt trauma victims with asymptomatic myocardial contusion (MC) who do not benefit from intensive cardiac monitoring, we prospectively divided 336 patients admitted to the SICU with possible MC following blunt trauma in the 6 years prior to January 1990 into three groups: Group 1 (n = 155, age 30.5 +/- 9 years) consisted of those patients admitted for mechanism of injury, J-point elevation, with or without minor chest injury. None developed arrhythmias. Their SICU length of stay (LOS) was 2.41 +/- 0.77 days. Group 2 (n = 43, age 31.5 +/- 10 years) patients had the same admission criteria as the patients in group 1 plus an abnormal emergency department ECG, i.e., arrhythmia, heart block, ischemia. None had cardiac complications. Their SICU LOS was 2.47 +/- 0.94 days. Group 3 (n = 138, age 40 +/- 20 years) patients had four or more rib fxs, a pulmonary contusion, a flail chest, or extra-thoracic injuries or were greater than 60 years of age. All required SICU admission for their non-cardiac injuries. Nineteen patients had cardiac complications requiring treatment. None had a cardiac death. Their SICU LOS was 10 +/- 22 days. We conclude that young patients with minor blunt thoracic trauma and a normal or minimally abnormal ECG do not benefit from cardiac monitoring.

Pathologic consequences of bilateral pulmonary lower lobectomies: case report.

Most injuries to the lung can be managed nonoperatively and rarely require resection. A case of bilateral hilar injuries requiring bilateral pulmonary lower lobectomies is presented. The resulting pulmonary hypertension, right ventricular failure, and cardiogenic shock explain the high mortality following extensive pulmonary resection in thoracic trauma and support the concept of a conservative approach.

Liver viability after ischemia-reperfusion.

Lack of a reproducible model to quantitatively assess hepatocellular injury following ischemia has made it difficult to assess new strategies for minimizing hepatic injury. We studied the progression of hepatocellular injury after ischemia and ischemia with reperfusion in rats. Irreversible injury was quantitated using a triphenyltetrazolium chloride assay that was shown to correlate with ultrastructural changes. Adenosine triphosphate decreased to 36% of basal values after 30 minutes, but returned to normal with reperfusion with no decrease in viability. In contrast, viability fell by 30% after 60 minutes of ischemia, and by 64% when 60 minutes of ischemia was followed by reperfusion. We conclude that reperfusion of ischemic liver increases the degree of irreversible damage. The model employed here seems to be useful for studying ischemic and reperfusion injury in the liver.