Outcomes after rib fractures in geriatric blunt trauma patients

Introduction

Rib fractures after blunt trauma contribute substantially to morbidity and mortality in the elderly.

Local effect of burn on skeletal muscle insulin responsiveness

Basal and insulin-stimulated glucose metabolism by skeletal muscle were studied 3 days after a 3-sec scald of one hindlimb of the rat. Soleus muscles from the burned and unburned limb of the burned rats, as well as from timed controls, were incubated with [U-¹⁴C]glucose and 0, 0.1, 1.0, or 10.0 mU insulin/ml. Basal glucose uptake by soleus muscle from the burned limb was 144% (P < 0.001) greater than that of the controls. The glucose uptake by muscle from the unburned limb did not differ from that of controls. Insulin increased glucose uptake in control and unburned muscles but had no effect in burned muscles. Basal lactic acid release by soleus muscle from the burned limb and the contralateral unburned limb of burned rats was 123% (P < 0.001) and 24% (P < 0.01) higher, respectively, than that of soleus muscle from control rats. Of the lactic acid released by muscles from control rats or the unburned limb of burned rats, 35% was derived from exogenous glucose. In contrast, 50–55% of the lactic acid released by muscles from the burned limb was derived from exogenous glucose reflecting a predominant conversion of glucose to lactic acid. Insulin had no effect on the rate of lactic acid release and did not change the proportion of glucose converted to lactic acid by any of the three muscle groups. The basal rate of glucose conversion to CO₂ by muscle from the burned limb was elevated 133% (P < 0.01) and that by muscle from the unburned limb was not altered as compared to controls. Insulin did not stimulate the conversion of glucose to CO₂ by any of the three muscle groups, and in the presence of insulin the release of CO₂ by burned, unburned, and control muscle did not differ. The basal rate of glucose incorporation into glycogen was the same in all three muscle groups. Insulin stimulated glucose incorporation into glycogen to a similar degree in muscles from control rats and the unburned limb of burned rats. However, the stimulatory effect of insulin was completely absent in soleus muscle from the burned limb. It is concluded that thermal injury suppresses the insulin-induced augmentation of glucose uptake and glucose incorporation into glycogen in skeletal muscles in the region of the burn but does not alter insulin sensitivity of skeletal muscles in the unburned region.     

Ultrastructure of the rat soleus muscle following a local scald injury

Previous studies demonstrated that 3 days after a 3-second scald of a hindlimb of a rat in 90°C water the soleus muscle of the burned limb, but not of the contralateral unburned limb, showed an elevated rate of in vitro glucose utilization and amino acid release. The aim of the present study was to correlate biochemical findings with the morphology of the muscle.Light and electron microscopic observations indicated that the thermal injury did not alter the structure of the proximal two-thirds of the soleus muscle from the burned limb. The distal part of the muscle exhibited inflammatory and degenerative changes. The extracellular space was dilated and numerous macrophages and fibroblasts were noted in the space. Patent blood vessels were rarely encountered and vessels exhibited varying degrees of endothelial damage. Muscle fibres showed a wide spectrum of morphological alterations. Some fibres appeared normal and others showed disruption of the organization of myofibrils. Some muscle fibres had degenerated, leaving a basement membrane-limited compartment which contained fragments of the muscle fibre and macrophages. Fibrin was noted both in the degenerating muscle fibres and in the extracellular space.It was concluded that soleus muscle from the burned limb is a heterogenous tissue containing both damaged and apparently normal muscle fibres, and non-muscle cells. The presence of macrophages and fibroblasts in the distal portion of soleus muscle could contribute to the increased rate of glucose utilization but further studies will be required to determine whether these cells are fully or only partially responsible for the metabolic alterations observed.     

Temporal alterations of intracellular Na,K, Ca,Mg, and PO4 in muscle beneath the burn wound

Three days after a single hindlimb scald in the rat, soleus muscle from the burned limb, but not from the contralateral unburned limb, shows an elevation in glucose uptake and utilization, an increase in protein turnover, and a loss of responsiveness to insulin. To assess the relationship of extra- and intracellular electrolyte concentrations to the changes, rats were scalded on one hindlimb and compared to controls at 4 hr, 1 day, and 3 days postburn. There were no pronounced changes in serum sodium, potassium, or calcium levels of burned rats. Serum concentrations of magnesium and phosphate, however, were elevated 4 hr postburn but were significantly lower than controls 3 days later. Intracellular electrolytes in soleus muscles from the unburned limb of burned rats were comparable to those in control muscles. In contrast, thermal injury resulted in profound intracellular electrolyte alterations in soleus muscles from the burned limb. Four hours postburn, the intracellular sodium concentration was elevated 210% (P < 0.001) whereas the concentrations of potassium, magnesium, and phosphate were reduced 44, 24, and 41% (P < 0.001), respectively. In the ensuing 3 days, all four ions returned to, or closely approached, the intracellular concentrations in control muscles. Unlike these transient alterations, thermal injury led in burned limb muscles to a progressive accumulation of cellular calcium reaching values 18-fold higher (P < 0.001) than control values 3 days postburn. The data suggest that this increase in cellular calcium could be linked to the chronic increase in glucose metabolism and protein turnover which develop in thermally injured muscle.     

Analysis of postburn insulin unresponsiveness in skeletal muscle

Three days after a one hindlimb scald in the rat, soleus muscle from the burned limb, but not from the contralateral unburned limb, fails to increase its rate of glucose incorporation into glycogen in response to insulin stimulation in vitro. Data presented indicate that the lack of response to insulin is not due to a release by thermally injured muscle of a substance that would either degrade insulin or decrease its biological potency. The insulin resistance is also not related to morphological changes in muscle because it is exhibited both by the portion of muscle that shows inflammatory and degenerative changes, and the portion of muscle that is electronmicroscopically indistinguishable from normal tissue. The insulin unresponsiveness cannot be reversed by addition of the ATP · MgCl₂ complex. The binding of insulin to its receptors in the intact soleus muscle from the burned limb does not differ from controls at 0.1 and 1.0 mU insulin/ml medium and is only 33% lower at 10 mU insulin/ml. This change in the capacity of thermally injured muscle to bind insulin is not of a sufficient magnitude to account for the complete lack of response to the hormone. Since in the absence of insulin, soleus muscle from the burned limb can convert glucose to glycogen and can respond to increased substrate availability by augmenting glycogen synthesis, the failure of muscle underlying the burn wound to respond to insulin appears to be due to a defect in coupling of the insulin receptor with intracellular effectors and/or in a component of the complex enzymatic machinery regulating glycogen metabolism.     

Chronic alterations in energy metabolism in the burned rat

Growth rates and food consumption were measured in rats following a non lethal scald burn on 26–28 per cent body surface to develop an animal model for studies of chronic metabolic alterations in the post burn recovery period. The injury was produced by immersing the dorsum of 235–260 g rats in 90°C water for 10 seconds. The burned animals grew at an attenuated rate compared to controls. At 11 weeks post burn, prior to the wound healing of the first rat, the burned animals weighed only 394 ± 10 g v. 494 ± 9 g (mean ± s.e.) in controls. At 42 weeks, when half of the animals healed, the body weight of healed rats (547 ± 16 g) was lower (P<0·05) than that of controls (618 ± 14 g), but greater (P<0·001) than that of their unhealed counterparts (426 ± 13 g). During the period from 42 to 63 weeks the weight of healed rats gradually approached that of controls (P<0·3) while the growth of unhealed animals was virtually arrested. During the first 10 days post burn, food consumption was diminished. However, in the subsequent period food intake per unit of body weight or body surface, which were linearly related for the weight range studied, was elevated in burned rats. At 11 weeks the corrected food consumption of burned animals was elevated 30 per cent (P<0·001). At 42 and 63 weeks, unhealed rats consumed 32 per cent (P<0·001) and 43 per cent (P<0·001) more per unit body weight or surface than corresponding controls. During this later period, the relative food consumption of healed animals became equal to that of controls. The persistently elevated food consumption per unit of body weight or surface suggests the development of hypermetabolism in burned rats. This similarity to burned patients may permit elucidation of factors controlling energy metabolism after thermal injury.     

Cardiopulmonary hemodynamics in patients with serious head injury

Cardiopulmonary hemodynamics after serious head injury were measured in eight patients to determine the relationship of these responses to intracranial pressure and alterations in pulmonary gas exchange. All patients had similar degrees of craniocerebral injury when assessed by the Glasgow Coma Scale, computerized tomographic scan, and initial intracranial pressure measurement. Intrapulmonary shunt fractions were elevated in all patients (range 11–29%) supporting the hypothesis that pulmonary dysfunction following isolated head injury is a distinct nosological entity. However, no correlation was found between level of intracranial pressure and any of the cardiopulmonary hemodynamic parameters studied. Patients surviving their injury initially showed a low cardiac index (2.56 ± 0.21 liters/min/M²) which subsequently became normal (3.77 ± 0.40 liters/min/M²). There was no evidence of increased pulmonary vascular resistance in these patients (95 ± 15 dyne-sec/ cm⁵). In contrast, patients dying of their injury generally had high pulmonary vascular resistance on admission (284 ± 74 dyne-sec/cm⁵) and a low cardiac index throughout their hospital course (1.87 ± 0.43 liters/min/M²). The cause of low cardiac index seen in this study is unknown. The abnormally high pulmonary vascular resistance in nonsurvivors may be a primary response of the pulmonary vasculature to serious head injury and reflect the severity of that injury.     

Vertical Axillary Thoracotomy: A Functional and Cosmetically Appealing Incision

Vertical axillary thoracotomy offers the specific advantages of minimum trauma and maximum preservation of chest wall function. A cosmetically acceptable scar results. The vertical axillary thoracotomy is specifically indicated in patients requiring less than the maximum intrathoracic exposure provided by the more traumatic posterolateral or anterolateral thoracotomy. The surgical technique is presented.     

Comparison of Operative Mortality and Morbidity for Initial and Repeat Coronary Artery Bypass Grafting: The Coronary Artery Surgery Study (CASS) Registry Experience

The National Heart, Lung, and Blood Institute's Coronary Artery Surgery Study (CASS) registry population was reviewed to allow comparison of operative mortality and morbidity rates for initial and repeat coronary artery bypass grafting (CABG) procedures. Standardized data collection was employed in CASS during patient entry (July 1, 1974, to May 31, 1979) and follow-up (ended November 30, 1982).Initial CABG was performed on 9,369 patients. Mean follow-up was 60.5 months. Repeat CABG was required in 283 patients (3.0%). The mean interval between operations was 39.3 months. Individuals needing reoperation tended to be young (p < 0.0001) and female (p < 0.002) and to have less extensive coronary artery disease (p ≤ 0.0001), less left ventricular impairment (p < 0.0001), less evidence of congestive heart failure (p = 0.006), and fewer coronary vessel systems bypassed at the first operation (p < 0.0001).Repeat CABG carried an increased risk of death compared with initial CABG (5.3% versus 3.1%, respectively; p < 0.05). However, the rates of perioperative myocardial infarction (6.4% for repeat and 5.8% for initial CABG) and of all surgical complications combined (30.6% versus 27.9%) were not significantly different from those at initial CABG.     

Surgical treatment of congenital esophageal atresia

Severe gastroesophageal reflux was found in 9 out of 18 infants with congenital esophageal atresia studied radiographically shortly after primary reconstruction. Pulmonary complications were recorded in 18 out of 32 similar patients in long-term follow-up. Strictures at the level of the anastomosis were detectable in 18 out of 32 patients; eleven strictures were severe enough to require dilation or surgical revision. These findings suggest that early evaluation for gastroesophageal reflux may be useful in management of infants with esophageal atresia. The precautions taken preoperatively to prevent complications of gastroesophageal reflux should be continued in the postoperative interval unless a competent lower esophageal sphincter is demonstrated.     

Anomalous Right Subclavian Artery Arising Proximal to a Postductal Thoracic Aortic Coarctation

Approximately 1% of patients with postductal thoracic aortic coarctation have an associated anomalous right subclavian artery. Previous reports indicated that the aberrant right subclavian vessel arose distal to the coarctation site. The case of a patient is presented in whom the anomalous right subclavian artery originated proximal to the postductal coarctation. We believe this to be among the first reports of this entity. The embryological development pathway and clinical implications of this congenital defect complex are discussed.     

Use of isovolemic hemodilution in the management of arterial ischemia in patients with polycythemia

The management of patients with both polycythemia and limb-threatening ischemia presents many difficulties because in this population, vascular surgical procedures carry a particularly high incidence of hemorrhagic and thromboembolic complications. We evaluated the use of acute isovolemic hemodilution in 12 polycythemic patients who required urgent surgery due to severe ischemia and threatened limb loss. Within 48 hours, blood was withdrawn in units of 500 ml and simultaneously replaced with 1,500 ml of lactated Ringer's solution until a hematocrit of 35 to 40 percent was achieved. After hemodilution, two patients had such a marked improvement that no further therapeutic measures were required immediately. Four patients showed definite improvement in pulmonary vascular resistance tracings and segmental Doppler pressures, but ischemia was not fully ameliorated. These patients together with the remaining six patients underwent vascular surgery within 1 to 14 days after hemodilution. A hematocrit of 32 to 40 percent was maintained during the perioperative period. All arterial reconstructions were successfully completed and there were no perioperative failures. No pulmonary emboli, myocardial infarctions, or deaths occurred in this period. These results indicate that in polycythemic patients, urgent vascular surgery can be performed more safely with the concomitant use of acute isovolemic hemodilution.     

Analysis of operative mortality after portal decompressive procedures in cirrhotic patients

One hundred thirty cirrhotic patients who had portal decompressive procedures were reviewed. Progressive hepatic failure, bleeding diathesis and shock or unsatisfactory operations accounted for the 90 day operative mortality of 36 percent. Many deaths occurred after emergency operations in which delay before surgery, increased operative time and intraoperative blood loss resulted in a higher incidence of hepatic failure and coagulopathy. Of the deaths related to unsatisfactory operations, technical difficulties resulting in massive hemorrhage, inadequate shunts and leaking gastrostomies were the causes. Of the various procedures, only the portacaval H-graft was not attended by any of the complications that resulted in massive intraoperative hemorrhage.Operative mortality may be reduced by early and expeditious operation in patients with actively bleeding cirrhosis, because massive blood loss and lengthy operations would result in further hepatic dysfunction because of splanchnic hypoperfusion. Of the standard total portal decompressive procedures, the portacaval H-graft may be the operation of choice because it precludes extensive venous mobilization while shunt adequacy and patency are excellent. Furthermore, decompressive gastrostomy is contraindicated in such patients. Reduction of operative mortality by such measures might result in a more realistic appraisal of long-term results in the surgical management of portal hypertension in patients with cirrhosis.     

Comparison of patency rate and structural changes of in Situ and reversed vein arterial bypass

We hypothesize that in situ vein may be a better arterial conduit than reversed vein. In order to evaluate this hypothesis, 47 in situ and 22 reversed vein bypasses from femoral to below knee arterial reconstructions were done for limb salvage and followed at 3-month intervals up to 30 months. Patients' age, sex, and run-off were similar in both groups. The cumulative patency rates at 12 and 30 months were 95 and 92% for the in situ group in contrast to 63 and 63% for the reversed group. These differences were significant (P < 0.01). This study was begun in a randomized manner, however, in situ vein bypass became the preferred procedure in the later part of the study. We further investigated the structural changes of in situ and reversed vein bypass in eight dogs. The left carotid artery was bypassed using in situ external jugular vein (ISV) and the right carotid artery was bypassed with reversed external jugular vein (RV) in each dog. These veins were examined by light and electron microscopy (scanning and transmission) prior to and at 1, 4, 8, 16, and 24 weeks following arterialization. At each interval RV showed endothelial disruption, degenerative changes, and progressive structural abnormalities similar to those of early atherosclerosis. In contrast, ISV showed minimal degenerative change, and underwent smooth transformation into a histologically appearing normal artery. This difference suggests that ischemia of the venous wall of RV may be responsible for the structural changes. The improved clinical patency rates seen with the in situ bypass may be explained by these experimental data.     

Further experience with visceral arteries as inflow sources

In eight patients in whom the traditional inflow arterial sources of the aortoiliac and axilliary arteries were unavailable for limb or visceral revascularization, the celiac and superior mesenteric arteries were successfully used. These proved to have satisfactory flow characteristics and to be easy to expose and use. Angiographic data suggest that the superior mesenteric artery is less frequently diseased at its origin than the celiac artery. No steal or redistribution problems were encountered.     

Polybrene neutralization as a means of monitoring heparin therapy for extracoporeal cirulation.

Dose-response effects of heparin and protamine in 34 adult patients undergoing cardiac operations were monitored by an in vitro analysis utilizing hexadimetharine bromide (Polybrene) neutralization. Heparin administered prior to cannulation for cardiopulmonary bypass in a dose of 3.0 mg (300 units) per kilogram of body weight, and 1.5 mg (150 units) per kilogram for each subsequent hour of bypass, routinely produced circulating heparin concentrations greater than 1.0 units per milliliter of plasma. A protamine dose equal to 80% of the total number of milligrams of heparin given resulted in no detectable plasma heparin in 23 of the 34 patients one-half hour after administration. No patient required protamine in an amount greater than the total number of milligrams in the heparin dose to achieve heparin neutralization. Modest postoperative chest tube drainage (mean, 784 ml in 48 hours) in these patients provides clinical support for low-dose protamine administration for heparin neutralization at the conclusion of cardiopulmonary bypass.     

Further experience with the saphenous vein used in situ for arterial bypass

Ongoing experience with use of the saphenous vein in situ as an infrainguinal arterial bypass is presented. One hundred eighty-three bypasses were performed for limb-threatening ischemia, 92 of which were to the popliteal artery, either isolated or in continuity with one or more tibial vessels, and 91 bypasses were carried to single tibial vessels below the termination of the popliteal artery. The results were analyzed by the life table method and show an overall patency rate of 89.8 percent at 3 to 4 years. Separate life table analysis of the tibial bypass group showed a patency rate of 83 percent at 3 to 4 years. Special emphasis is placed on the ability to use veins less than 4 mm in diameter, which comprise 40 percent of those used in these procedures. The superior results provided by the in situ method are explained in part by experimental observations which show that endothelial stability is completely preserved by this method but is severely disturbed during the process of vein removal and reversal.     

Entrapment of the median nerve and flexor pollicis longus tendon in an epiphyseal fracture-dislocation of the distal radioulnar joint: a case report

A 10-year-old boy sustained a severe distal radius and ulna epiphyseal fracture-dislocation, Salter type II, with entrapment of the median nerve and the flexor pollicis longus tendon. Nerve function was intact before reduction and is normal 1 year after open reduction.