Tube feeding: new life for an old procedure.
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Critical Illness↗
Biomedical subjects
C W Van Way
Publications and source records attributed to C W Van Way.
The use of insulin and glucose during resuscitation from hemorrhagic shock increases hepatic ATP.
BACKGROUND: Hemorrhagic shock produces a marked decrease in hepatic ATP, adenylate energy charge, and total adenosine nucleotides. This is followed by slow recovery to normal levels after resuscitation. Nucleotide metabolites are increased following shock and resuscitation. Previous experimental work has shown that supraphysiologic doses of insulin have salutary effects in animals with hemorrhagic shock and in cardiac patients. It appears that insulin causes increased availability of glucose and energy-producing substrates. This study examined whether resuscitation with glucose and insulin after hemorrhagic shock would alter the changes previously seen to occur in hepatic ATP levels, adenylate energy charge, or nucleotide metabolites. METHODS: Male Sprague-Dawley rats were bled to a mean arterial blood pressure of 40 mm Hg for 30 min. They were then resuscitated with the shed blood and one of three fluids: (1) lactated Ringer's, (2) lactated Ringer's with 10% glucose, (3) lactated Ringer's with 10% glucose + 6 units/kg regular insulin. Liver biopsies were obtained prior to shock (baseline), after 30 min of shock (shock), and 90 min after resuscitation (90 min). Tissue levels of ATP, ADP, AMP, adenosine, inosine, hypoxanthine, and xanthine were measured. Serum at 90 min was evaluated for potassium, glucose, and tumor necrosis factor alpha (TNF-alpha). RESULTS: The insulin-treated group had significantly increased hepatic ATP and energy charge following resuscitation compared with the other two groups. The insulin group also exhibited significant hypoglycemia. Total adenine nucleotides (ATP, ADP, and AMP) were significantly elevated 90 min postresuscitation in the insulin group. Mean blood pressures throughout the experiment were not significantly different among groups. TNF-alpha was highest in the insulin-treated group, but this was not significant. CONCLUSIONS: Resuscitation with insulin and dextrose significantly increased hepatic ATP and adenylate energy charge after hemorrhagic shock in rats. Total nucleotide pool levels were not different between groups, indicating that there was a shift of the equilibrium away from the metabolites toward ATP and ADP in the insulin-treated group. Insulin treatment had no significant effect on blood pressure or TNF-alpha. However, it caused significant hypoglycemia and hypokalemia.
Adenosine Diphosphate↗
Low falls: an underappreciated mechanism of injury.
OBJECTIVE: This is a retrospective study designed to evaluate the pattern and severity of injuries that result from low falls, defined as falls from less than 20 ft, subsequent mortality, and requirements of hospital resources. Our hypothesis is that many of these injuries, even without cardiopulmonary instability, are worthy of trauma center care. METHODS: The records of all patients entered into the hospital trauma registry at an urban Level I trauma center during the years 1991 through 1997 who suffered low falls and who either died after admission or were hospitalized for at least 3 days were reviewed. Patients suffering isolated hip fractures were excluded. One hundred seventy-six patients constituted the study population. This group accounts for about 2% of all admissions for falls at our institution. Patterns of injury were examined. Age, mechanism of injury, Injury Severity Score (ISS), and cardiopulmonary or neurologic instability on admission were documented. Mortality, length of intensive care unit and hospital stays, as well as billed hospital charges, were reviewed. RESULTS: The majority of patients (62%) were younger than 50 years. Sixty patients had ISS >15 and 116 patients had ISS >9. Sixty patients had multisystem injuries requiring specialty care. Head injuries were found in 81 patients (35%), and vertebral fractures or spinal cord injuries were found in 49 patients (22%), including 9 quadriplegics and 5 paraplegics. There were seven patients with intra-abdominal injuries (five spleen and two bowel injuries). There was one patient with a rupture of the thoracic aorta. Seventeen patients had deteriorating neurologic or pulmonary function on arrival, but the majority (90%) were stable. Of the 159 "stable" patients, 48 suffered head injuries, 7 were quadriplegic, and 3 were paraplegic. All intra-abdominal injuries were in this group. Overall, 14 of 176 patients (8%) died. Seven deaths were in patients older than 60 years, and seven deaths were in younger patients (p = 0.04). The majority of deaths (9 of 14) were from head trauma. Care in the intensive care unit was required in 92 of 176 patients. Nine patients had billed charges exceeding $100,000. CONCLUSION: Low falls can cause significant injuries, most commonly to the head and spine. Based on mechanism of injury alone, patients injured in low falls might not be taken to trauma centers. We have found, however, that many of these patients sustain serious multisystem injuries, even though they are stable initially. Although these patients represent only a fraction of those who fall, our study would support adjustment of triage guidelines to recommend transport of such patients, particularly elderly patients, to trauma centers.
Accidental Falls↗
Infectious sequelae in the use of polyglycolic acid mesh for splenic salvage with intraperitoneal contamination.
Salvage of the injured spleen is important in the trauma patient. Loss of the spleen can result in both early and late infectious complications due to immunologic and phagocytic deficits. Splenic salvage techniques include the use of polyglycolic acid (PGA) mesh to wrap and tamponade the damaged and bleeding spleen. However, the use of mesh may increase the incidence of infection in the presence of intraperitoneal contamination. We examined whether mesh in the contaminated field increases the infection rate compared to splenectomy in a murine model. Sixty male Sprague-Dawley rats were divided into three groups of 20 each: splenectomy, splenic wrap with PGA, and control (with splenic mobilization). All rats were subjected to a standard inoculum of enteric bacteria at the time of celiotomy. Sixteen (80%) of the splenectomy rats, 10 (50%) of the PGA mesh wrapped rats, and four (20%) of the control rats expired (P < 0.5). In surviving rats, necropsy at 7 days demonstrated abscess formation in all four (100%) of splenectomy, four of 10 (40%) in PGA mesh wrapped, and two of 16 (13%) of control rats. All of the abscesses in the wrap group involved the mesh. Overall infection rates (including fatal peritonitis, abscess formation, and empyema) were 100% for splenectomy, 75% for PGA mesh wrapped, and 30% for control rats (P < 0.05). We conclude in this experimental model that the use of PGA mesh wrap does increase susceptibility to infection, but much less so than splenectomy in the presence of intraperitoneal contamination.
Abscess↗
Changes in adenine nucleotides during hemorrhagic shock and reperfusion.
Certain tissues are known to be susceptible to shock-induced damage: liver, small bowel mucosa, and small bowel wall. This study was done to assess the changes in adenine nucleotides induced by hemorrhagic shock. Male Sprague-Dawley rats (n = 21; 300-350 g) were anesthetized with sodium pentobarbital (50 mg/kg, ip) and mechanically ventilated. The external jugular vein and common carotid artery were cannulated. Laparotomy was done. Hemorrhagic shock was induced by withdrawing blood into a heparinized syringe until a mean arterial blood pressure of 40 mm Hg was obtained and was maintained for 30 min by continued withdrawals. Shed blood was then reinfused through the venous catheter. No additional fluid was administered. The animals were observed for another 60 min. Throughout the procedure, biopsies were taken of liver and small bowel. The small bowel biopsies were separated into mucosal and wall fractions. Nucleotides were extracted. ATP, ADP, AMP, adenosine, inosine, xanthine, and hypoxanthine were measured with gradient HPLC. Cellular ATP concentrations decreased significantly during shock (P < 0.05). Liver ATP dropped from 8.93 +/- 0.55 to 2.91 +/- 0.16 micromol/g dry tissue (mean +/- SEM) (33%), small bowel mucosal ATP from 9.40 +/- 1.04 to 3.26 +/- 0.21 (35%), and small bowel wall ATP from 5.47 +/- 0.36 to 2.74 +/- 0.18 (50%). The nucleotide response to shock in small bowel mucosa was closer to that of liver than to that of small bowel wall. After reperfusion, ATP levels were partially restored in liver, small bowel mucosa, and small bowel wall, but not to preshock values. All of the metabolites (adenosine, inosine, hypoxanthine, and xanthine) increased during shock (P < 0.05), and did not return to preshock levels after reperfusion. The abnormalities in ATP and its metabolites, and their persistence after reperfusion, suggest a possible mechanism for the production of postshock damage.
Adenine Nucleotides↗
National Coordinating Committee for Nutrition Standards clinical indicators of nutrition care.
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Dietetics↗
Peripheral nerve elongation with tissue expansion techniques.
Elongation of peripheral nerves would facilitate the repair of peripheral nerve injuries. The purpose of this study was to determine the efficacy of nerve expansion and the effect of different levels of intraluminal expander pressure upon nerve conduction. A 2-mL Silastic expander was placed under one sciatic nerve of adult male rats. The other nerve served as a control. Electroneuromyography (ENMG) was done at the time of initial expansion in seven animals. At 40 mm Hg expansion pressure a significant change in latency was found with an increase of 17% +/- 5%. Expansion was carried out for 14 days in two groups of seven rats, group I at 20 mm Hg and group II at 40 mm Hg. Length gain on the expanded side was 30% in group I and 40% in group II. No significant changes in latency or velocity were found after expansion. We conclude that nerves can be expanded at low pressures with no significant conduction changes but long-term recovery of histologic changes needs to be evaluated.
Animals↗
A prospective study of incisional time, blood loss, pain, and healing with carbon dioxide laser, scalpel, and electrosurgery.
Carbon dioxide laser incisions are reported to be less painful, less bloody, and less prone to seroma formation and to heal better than scalpel or electrosurgical incisions. We compared all three modalities in a prospective randomized study of cholecystectomy incisions. Time required for the incision and incisional blood loss was less with electrosurgery than with the carbon dioxide laser or scalpel. Postoperative pain and wound healing, however, were the same for all three techniques. The carbon dioxide laser appears to offer no advantage over conventional means of making a standard incision.
Adult↗
Nutritional support in the injured patient.
After injury, the stress reaction causes hypermetabolism and consequent depletion of the body's tissues. Nutritional support should be begun early and should be given by the enteral route if possible. New developments may allow the modulation of the stress and immune responses by nutrient therapy.
Burns↗
Intrathoracic and intravascular migratory foreign bodies.
Intrathoracic and intravascular migratory foreign bodies are a small but distinctive subgroup of missile injuries. The intravascular bullet embolus can be treated like arterial or venous emboli of any other sort and removed as indicated. Wandering bullets in body cavities should be removed when they need to be, just like bullets imbedded in the body in a fixed position. And, contrary to the popular belief, very few bullets wander.
Blood Vessels↗
Advanced techniques in thoracic trauma.
Technologic aid is available for the three central problems of hemorrhage, lung damage, and cardiac damage. Autotransfusion, new modes of ventilator support, extracorporeal oxygenation, balloon pumping, and left ventricular assist are available for the trauma patient. The author explains these new devices and their role in thoracic trauma cases.
Assisted Circulation↗
Detection thresholds of nonocclusive intestinal hypoperfusion by Doppler ultrasound, photoplethysmography, and fluorescein.
Because clinical assessment of bowel viability is unreliable, other methods of determining intestinal perfusion have been recommended. Since none of these quantifies intestinal blood flow, we measured flow at the detection thresholds of Doppler ultrasound, photoplethysmography, and intravenously administered fluorescein, perfused the intestines at these threshold levels, and assessed histologic evidence of ischemic damage. The intestines of five anesthetized dogs were perfused for 4 hours via an in-line pulsatile extra-corporeal circuit assembled between the iliac and superior mesenteric arteries at either relatively physiologic (approximately 20 ml/min/kg body weight) levels or reduced levels representing the flow detection thresholds of Doppler ultrasound or photoplethysmographic probes (approximately 4 ml/min/kg). Intravenously administered fluorescein was detected at even lower perfusion levels (approximately 2.1 ml/min/kg). Clear-cut ischemic changes were documented histologically in all subjects perfused at Doppler/PPG flow detection thresholds but in none of those perfused at normal levels. We conclude that threshold blood flow detection by any one of these methods, especially fluorescein, occurs at levels inadequate to guarantee tissue viability.
Animals↗
Cardiac dysrhythmias in the acute setting: pathophysiology or anyone can understand cardiac dysrhythmias.
Cardiac dysrhythmias are easy. Unlike the lung (which has formidable neuroendocrine, metabolic, and respiratory responsibilities), the heart is simple. It is an innervated muscular pump. A resting Purkinje or ventricular muscle cell membrane maintains a charge of about 90 millivolts. The five phases of a cardiac action potential are similar to the action potential in skeletal muscle, however, the cardiac action potential lasts a hundred times longer. When sodium specific "fast" channels and calcium specific "slow" channels open, positive ions rush into the myocardial cell, thus causing rapid membrane depolarization. In order to produce an action potential, some stimulus must decrease the membrane potential from -90 millivolts to "threshold" or -60 millivolts. Purkinje fibers do not have a stable phase for diastolic potential. These fibers continuously depolarize during diastole. Hypoxemia or hypokalemia may exacerbate this diastolic depolarization, thus promoting "hyperexcitability" or "automatic" ectopy. When myocardium is damaged, characteristically with myocardial ischemia, rapid conduction of cardiac impulses may be slowed dramatically. Very slow impulses may course through muscle such that by the time the activation wave front returns to the initiating site, this origin has had a chance to repolarize. This is the basis for re-entrant dysrhythmias. All cardiac dysrhythmias are automatic, re-entrant or both.
Arrhythmias, Cardiac↗
Cardiac dysrhythmias in the acute setting: recognition and treatment or anyone can treat cardiac dysrhythmias.
The two primary goals in dysrhythmia therapy are: to control the ventricular rate (between 70 and 100 beats per minute) and to maintain sinus rhythm. Maintenance of sinus rhythm is definitely secondary. If a patient is hemodynamically unstable, but has a ventricular rate between 60 and 100 beats per minute, the trouble is almost certainly not due to the cardiac rhythm. Normal conduction velocity is fast. An impulse is transmitted by healthy Purkinje fibers at 2 to 3 meters per second. This means that the entire ventricle, when activated by the Purkinje system, is activated in 80 milliseconds. When a superventricular impulse is transmitted to the ventricles via the A-V node, the ventricle should be activated (depolarized) in less than 80 milliseconds. Conversely, if an impulse is generated at an ectopic ventricular site, it does not access the high velocity Purkinje system as rapidly. A ventricular origin beat (PVC) thus, takes longer to activate the entire ventricle. The QRS is, therefore, longer (or wider). A wide QRS signifies aberrant ventricular conduction. When a dysrhythmia originates above the A-V node, the therapy is pharmacologic A-V nodal blockade (verapamil). When a dysrhythmia originates below the A-V node, therapy is pharmacologic (Lidocaine) or electrical (cardioversion). If uncertain or a patient is unstable, cardioversion is always acceptable. Thus; with an unstable patient, proceed immediately to cardioversion; with a narrow complex tachycardia (superventricular) proceed to verapamil; and with a wide complex (ventricular) tachycardia give Lidocaine and proceed to cardioversion.
Arrhythmias, Cardiac↗
Prevention of suction-induced gastric mucosal damage in dogs.
Gastric suction has traditionally been available in three modes: continuous, sump, and intermittent. An intermittent air injection suction system (IAIS) has been developed in which small (20 to 30 mm) amounts of air are injected two to three times a minute. Very low (20 mm Hg) suction levels are applied. The hypothesis of the present study is that such a device will prevent suction-induced gastric mucosal damage, probably produced by suctioning of mucosa into the holes of the NG tube. IAIS should prevent this by physically expelling the mucosa out of the holes and allowing use of much lower suction levels. In 25 animals, gastric suction for 24 h in anesthetized dogs routinely produced ulcers. However, IAIS produced significantly fewer ulcers and in fewer animals. In 37 animals, the effectiveness of suction, measured by recovery of fluid instilled in the stomach, and the tendency of the tube to block were studied. Effectiveness was the same for all modes studied. Blockage was significantly less with IAIS.
Air↗
Aortocardiac fistula with aortic valve injury from penetrating trauma.
A patient with a delayed aorto-right ventricular fistula and aortic valve injury after penetrating trauma is reported, and 17 similar additional cases from the literature reviewed. By examining the aortic root of adults with normal cardiac anatomy at autopsy, we defined the target area for these injuries as a 2 X 2 cm contact surface between the aorta above the right coronary cusp and the right ventricular outflow tract below the pulmonary valve. Five of the 18 patients required emergency exploration due to hemodynamic instability. Life-threatening sequelae (hemorrhage and cardiac tamponade) result from the external injury rather than the intracardiac component. Intracardiac damage is most commonly manifested as the delayed recognition of a cardiac murmur and some degree of congestive heart failure, and when these appear one must suspect intracardiac trauma. We recommend cardiac catheterization and elective repair, maintaining control of both ends of the intracardiac fistula with bolstered suture. Aortic valve injury can often be primarily repaired. Patients with combination aortic valve and aortocardiac fistula injuries, more so than those with a single intracardiac lesion, fail with nonoperative management. Of the 18 patients, 17 underwent surgery. One of these died: the others did well during short-term followup (less than 1 year).
Adolescent↗
Delayed staple penetration of the heart: transthoracic migration with late tamponade.
Most foreign bodies in the chest do their damage at the time of injury. While needle-like objects may migrate (6), delayed intrathoracic injury is rare. Delayed transthoracic penetration of the heart by a staple is reported, and is felt to be unique because acute hemopericardium resulted 30 days after the time of initial injury. The principles of recognition of pericardial tamponade, initial stabilization with periocardiocentesis, and immediate exploration are emphasized.
Adult↗
The protective action of allopurinol in an experimental model of haemorrhagic shock and reperfusion.
Haemorrhagic shock was induced in anaesthetized, open-chest dogs by controlled arterial bleeding, sufficient to reduce and maintain mean arterial blood pressure at 40 mmHg for 30 min. The blood volume was then restored to the pre-shock level by rapid, intravenous reinfusion of the blood shed during the shock period. Haemorrhagic shock produced significant haemodynamic changes, characterized by a marked depression of myocardial function. Cardiac output (1226 +/- 57 ml min-1), peak aortic blood flow (6030 +/- 383 ml min-1) and maximum rate of rise of left ventricular pressure (2708 +/- 264 mmHg s-1) were all reduced by more than 50%. The haemodynamic profile was markedly improved by reinfusion of shed blood but this improvement was not sustained. There was a gradual decline such that 50% of the untreated animals suffered complete circulatory collapse and death between 60 and 120 min following reinfusion. Neither haemorrhagic shock, nor reinfusion of shed blood produced any consistent or significant changes in the myocardial adenine nucleotide pool. The ATP, ADP and AMP levels were, respectively, 25.9 +/- 4.2; 15.6 +/- 1.0; 4.3 +/- 1.9 nmol g-1 protein, before haemorrhagic shock; 21.6 +/- 3.4; 21.5 +/- 2.5; 10.2 +/- 2.7 nmol g-1 protein, after 30 min haemorrhagic shock; and 29.9 +/- 3.9; 16.5 +/- 1.2; 4.2 +/- 1.1 nmol g-1 protein, 60 min following reinfusion of shed blood. Pretreatment with allopurinol (50.0 mg kg-1 i.v.), 60 min before inducing haemorrhagic shock, had no significant effect upon the haemodynamic response to shock, but did prevent the gradual decline seen following reinfusion in the untreated animals. All of the allopurinol-treated animals displayed significantly better haemodynamic profiles than the untreated animals, furthermore, there was a 100% survival rate in this group. 5 Allopurinol had no significant effect upon the myocardial adenine nucleotide pool either during haemorrhagic shock or following reinfusion of shed blood.
Adenine Nucleotides↗