Biomedical subjects
Publications and source records attributed to G T Shires.
Diabetes insipidus was encountered in a 58-year-old woman after injury in an closed space fire. Carboxyhemoglobin measured 26% after 30 minutes of assisted ventilation with an FIO2 of 1.0. The failure of antidiuretic hormone was a sign of a diffuse cerebral insult caused by carbon monoxide poisoning. The hormonal deficit was easily corrected by exogenous vasopressin. Mortality was related to the cerebral lesion.
The results of this prospective clinical study have demonstrated a low rate of false-positive abdominal sonographic findings in patients undergoing routine studies the seventh day after abdominal surgical procedures. It is concluded that any intraperitoneal fluid collection detected by ultrasound examination in a patient postoperatively demonstrating signs and symptoms of abdominal sepsis (fever, leukocytosis, pain, tenderness, persistent ileus, excessive drainage, wound changes and so on), should be considered as the source, as abdominal fluid collections do not persist as a "normal" part of the healing process one week after extensive biliary tract or colonic operations. Sonography is a highly specific procedure for the detection of abdominal abscesses after the seventh postoperative day. The type of procedure, type of incision, type of closure, presence of drains, history of prior intraperitoneal surgical procedures and operative blood loss did not affect the accuracy of the test. Postoperative ultrasonography is a specific, sensitive and accurate test and is widely applicable to almost all groups of patients.
A technique has been described which allows replacement of endotracheal tubes, while maintaining control of the airway, using a fiberoptic bronchoscope. The technique was successful in 27 of 29 attempts. While this method does not replace elective tracheostomy, it is indicated for critically ill patients requiring urgent replacement of endotracheal tubes in whom anatomic considerations preclude conventional methods.
The results of this study demonstrated that muscle ATP levels were sustained in hemorrhagic shock despite marked deterioration of muscle function as indicated by a decline in PD. This indicated that energy depletion was not the primary basis of the cellular dysfunction in hemorrhagic shock. Cellular dysfunction and metabolic abnormalities in the liver occurred earlier during the course of hemorrhagic shock than in muscle. Other studies were cited in which it was suggested that inhibition of the membrane bound sodium and potassium active transport mechanism is the likely cause of tissue electrolyte and fluid shifts observed during prolonged periods of hemorrhagic shock.
A simultaneous comparison of the effect of partial and total ischemia on skeletal muscle was made in dogs. The totally ischemic muscle had larger changes in adenosine triphosphate (ATP), creatine phosphate (CP), and cellular transmembrane potential difference (PD) during the 3-hour ischemic period than the partially ischemic muscle. Following recovery, all measured parameters in the totally ischemic muscle returned to normal, but paradoxically the PD in the partially ischemic muscle remained depressed despite the return to normal levels of ATP and CP. Contrary to the results in partially and totally ischemic brain tissue there was no evidence for higher levels of lactic acid in the partially ischemic muscle that could explain the persistent alteration in muscle cell function.
A group of 30 burn patients with 36-87% total body surface area (TBSA) burns was studied at 24-48 hr postburn. These included studies of (1) autologous and allogeneic mixed-lymphocyte reactions (MLR); (2) the immunoregulatory influence of mitomycin C-treated T cells, non-T cells, and unfractionated peripheral blood lymphocytes (PBL) on allogeneic MLR; and (3) correlation between the proportions of T-cell subsets defined with monoclonal antibodies (OKT4 and OKT8) and autologous MLR. Studies concerning adherent cell production of thromboxane, prostaglandin E2, and prostaglandin F2a and the immunomodulatory effects of Interleukin 1 (IL-1), Interleukin 2 (IL-2), and a prostaglandin inhibitor, WY-18251, on autologous MLR are presented. The autologous mixed-lymphocyte reaction was depressed in 60% of the burn patients tested. This depressed response correlated closely to the extent of third-degree injury (P less than 0.025) and to TBSA injury greater than 60% (P less than 0.025). A linear correlation was observed between the depression in autologous MLR and a decrease in both the percentage of OKT4+ T cells and the OKT4+/OKT8+ ratio. The response of T cells from burn patients in allogeneic MLR was normal. Age, sex, TBSA of the burn, and size of second-degree burn did not correlate with the abnormalities observed in MLR. Mitomycin C-treated mononuclear cells, purified T cells, or non-T cells from burned patients did not demonstrate any suppressive influence on MLR in normals. Monocyte number and arachidonic acid metabolism were investigated. In addition to increased numbers of monocytes following thermal injury, adherent cells produced increased quantities of thromboxane, prostaglandin E2, and prostaglandin F2a. The effects of Interleukin 1, Interleukin 2, and a prostaglandin inhibitor, WY-18251, were studied in autologous MLR (AMLR) of burned and normal patients. Interleukin 1 and WY-18251 did not induce any significant changes in proliferation in burned patients or normal controls. When compared to cultures without exogenous IL-2, an increase in AMLR was observed following the addition of IL-2 to burn patient cultures at Day 6 and Day 7 of culture. Although the addition of IL-2 did increase proliferation in AMLR of normal controls at Day 6 and Day 7, the enhancement observed for the burn patient cultures represented a restoration to the level of normal control cultures without IL-2. A dose-dependent increase in AMLR was observed in T cells isolated from normal and burned patients in the presence of purified Interleukin 2.(ABSTRACT TRUNCATED AT 400 WORDS)
Several theories have been advanced in an effort to explain immunologic suppression after thermal injury, that is monocyte production of immunoregulatory prostaglandins, activation of suppressor cells, production of suppressive serum factors and alteration in helper cell function. In the current study, cytofluorometric analysis was performed on peripheral blood mononuclear cells isolated from 30 severely burned individuals using a FACS IV cell sorter. Fluorescein labeled monoclonal antibodies were used to phenotype total T cells (OKT3+), helper cells (OKT-4+), suppressor cells (OKT-8+), monocytes (antimono.2+) and B cells (anti-Ia+). After burn injury, the most striking phenotypic alterations observed were a marked decrease in the number and percentage of total OKT3+ T cells and OKT4+ helper cells. No significant increases were observed in the OKT8+ suppressor cell subpopulation. Monocytes exhibited a transitory increase during the first 48 hours postburn which returned to normal by postburn day 7. The percentage of Ia+ cells were either normal or decreased in number during the course of the injury. An OKT-4 to OKT-8 ratio of less than 1.00 at 24 to 48 hours postburn may represent a reliable predictive index for death by sepsis. These data suggest that the syndrome of burn induced immunologic suppression may be better described as a "burn induced immunodeficiency syndrome," that is characterized by decreased numbers or function of Interleukin-2 producing helper cells, or both.
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Following distal arterial and venous cannulations in both hind limbs of 10 dogs, left leg arterial pressure was reduced to less than 50 torr (group I) and 50 to 75 torr (group II). Muscle membrane potential difference (PD) measurements, muscle biopsies, and arterial and venous blood samples were taken at baseline, after 3 hours of ischemia, and following 3 hours of reperfusion. Blood gas tensions and blood and muscle metabolites were measured. Muscle creatine phosphate levels fell during the ischemic period, but the adenosine triphosphate concentration remained normal. The PD fell in both groups during ischemia and declined further after reperfusion (p greater than 0.01). The deterioration in cell membrane function occurred in spite of intracellular energy repletion and persisted after reperfusion. The PD appears to be a more sensitive indicator of ischemia-induced cell dysfunction than levels of blood or intracellular metabolites. The cause of the progressive fall in the membrane potential is uncertain, but it may be due to cytotoxicity produced by oxygen free radicals.
Epidermal cells from cadaver skin grown in culture into confluent sheets of stratified cells were grafted on to partial thickness burn wounds in three patients. The burn areas covered with these allogeneic cultured epidermal allografts were tangentially excised deep second-degree burns which routinely would have been covered with split-thickness autografts. The burn wounds grafted with cultured allografts healed within three days and remained healthy for the 9 months of observation. Since epidermal cell cultures may be grown continuously, cultured allografts may serve as alternative biological dressings, or grafts, for deep second-degree burn wounds. They produce accelerated healing and an excellent cosmetic result, and they reduce the need for split-thickness autografts.
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The effect of Ringer's Lactate (RL) and a colloid containing salt solution Plasmanate (PL) on extravascular lung water (EVLW) during aortic surgery was evaluated in a prospective study of 18 patients. Measured blood loss was replaced with packed red blood cells. In addition to red blood cell replacement, either RL or PL was infused (1) to maintain the cardiac output (CO) equal to or greater than the preoperative value, (2) to maintain the pulmonary capillary wedge pressure (PCWP) plus or minus 2 mmHg of preoperative values, and (3) to keep the urinary output greater than or equal to 30 cc/hr. Cardiac output, EVLW, PCWP, serum colloid osmotic pressure (COP), and intrapulmonary shunt fraction (Qs/Qt) were measured serially. All baseline values were similar between groups. The groups were well matched for age, associated disease, operating time, blood loss, and blood transfusions. During operation, the RL group required two times the rate of infusion of the PL group. Urine flow rates were similar on the day of surgery, but by postoperative days one and two, the PL group had approximately one-half of the urine flow rate compared to the RL group. Cardiac output and Qs/Qt increased in both groups. EVLW did not change after operation in either group, despite marked decrease in COP in the RL group. These data indicate that crystalloid resuscitation to physiologic endpoints does not increase extravascular lung water. Thus, manipulation of COP by PL was unnecessary in these patients.
Septic shock was induced in adult baboons by the infusion of live Escherichia coli. A progressive derangement in skeletal muscle cell function was documented by the direct measurement of declining transmembrane potential difference (PD). A concurrent depolarization of the red blood cell (RBC) was characterized by cellular uptake of chloride, sodium, and water, and loss of potassium. The decrease in RBC PD was significantly greater than the change predicted to occur from acidosis alone. These findings are compatible with changes in membrane permeability and decreased active transport. The continuous accumulation of RBC adenosine triphosphate during shock suggests decreased energy utilization rather than decreased energy production as a factor leading to diminished active ion transport.
Transmembrane potential difference (PD) is a reliable indicator of cellular function. Decreased PD in hepatocytes in hemorrhagic shock occurred concomitant with decreased adenosine triphosphate (ATP), suggesting energy depletion as the mechanism of cell dysfunction. This study correlates changes in liver and muscle PD with hepatocyte ATP, glucose-6-phosphate (G-6-P), and lactate levels in burn shock and resuscitation. Six adult female baboons were subjected to 52.4 +/- 6.3% body surface area third-degree scald burns. The animals were resuscitated using the Parkland formula, after the muscle PD had fallen to -70 mV. Liver PD decreased from 46.2 +/- 2.4 mV to 22.4 +/- 3.8 mV in burn shock. The PD recovered toward normal with resuscitation. ATP and G-6-P contents did not change significantly, while lactate rose threefold in burn shock. A severe cellular derangement was indicated by this marked hepatocyte depolarization. Maintenance of normal intracellular ATP excludes energy depletion as the mechanism of this cell dysfunction. These findings are consistent with failure of active ion transport or changes in cell membrane permeability which were partially recovered during fluid resuscitation.
Ten cases of pancreaticoduodenectomy (PD) performed for benign disease are reported with all patients alive and well at an average of 7.5 years. A review of the English literature reveals that 52 patients have had a PD for benign disease in which a carcinoma had originally been suspected (incidence of 1%) with an overall surgical mortality of 9.6%. Three hundred and thirty-four cases of PD done for complications of pancreatitis have been reported with an overall mortality of 4.8%. On rare occasion, despite extensive preoperative evaluation, a patient will be explored with true uncertainty as to the diagnosis of a periampullary mass. Under these circumstances, it has been considered good surgical judgement to proceed with resection, considering that the lesion may be benign, as opposed to leaving behind an early resectable malignant lesion. Results of this review support this policy only in that if the PD is done for what turns out to be benign disease, the perioperative mortality is low, and an excellent long-term survival can be expected.
Sepsis continues to be a major cause of patient death following hemorrhagic shock. To explain this increased susceptibility to infection on a cellular level, neutrophil function was studied in nine adult baboons subjected to severe hemorrhage. Neutrophil migratory activity was found to be significantly decreased immediately after hemorrhage (P less than 0.05 vs control) and continued to decline throughout the experiment. After an initial small decline, neutrophil adherence increased to significant levels after 4 h of hypotension (P less than 0.05 vs control). The present data support the hypothesis that increased susceptibility to infection after sustained hemorrhage is a result of impaired neutrophil function.
In the last ten years anaerobic organisms have emerged as the major infecting agent in surgical patients. While these groups of organisms including Bacteroides fragilis, clostridia, and anaerobic cocci persist, there has, in addition, developed in the last few years a virulent group of nosocomial infections, and modern management of sepsis is primarily directed at gram-negative and anaerobic infections, which include nosocomial infections, for example, those caused by the Serratia group. Much has been learned about control of infections from the patient who has sustained thermal injury. While topical water-soluble antibiotics have been a remarkable advance in the care of the burn patient, systemic and subeschar antibiotics have proved essential in the management of severe burn injury. There is increasing evidence that there is remarkable interference with host defense mechanisms in patients who have sustained burns or significant trauma or intraabdominal infection. The patient sustaining nonthermal traumatic injury also sustains reduction in host resistance. Because of this and the additional initial contamination, in the traumatized patient antibiotic therapy should be started early and as a therapeutic measure. Newer localization techniques, including sonography and computed axial tomography scanning, have helped localize abdominal infections early. Specific antimicrobial therapy may be begun as an adjunct to the surgical therapy of intra-abdominal infection.
Pulmonary acid aspiration results in hypoxemia and hypovolemia. We assessed the effects of positive end-expiratory pressure (PEEP) and fluid resuscitation on oxygenation and alveolar-capillary membrane permeability after acid aspiration. Alveolar-capillary membrane permeability was assessed by determination of extravascular lung water volume, using the thermal-green dye double-indicator technique, extravasation of iodinated 1 125 serum albumin into lung parenchyma, and albumin leak into the alveolar spaces. The data from this study demonstrated that PEEP improved oxygenation after acid aspiration, but did not alter progression of the injury; cardiac output and oxygen transport were improved by plasma volume repletion while receiving PEEP; and resuscitation with 5% albumin solution increased plasma albumin content and tracheal albumin content commensurately and did not modify progression of the injury.