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We studied prospectively the regional inflammatory response to a unilateral distal radial fracture in 114 patients at eight to nine weeks after injury and again at one year. Our aim was to identify patients at risk for a delayed recovery and particularly those likely to develop complex regional pain syndrome. In order to quantify clinically the inflammatory response, a regional inflammatory score was developed. In addition, blood samples were collected from the antecubital veins of both arms for comparative biochemical and blood-gas analysis. The severity of the inflammatory response was related to the type of treatment (Kruskal-Wallis test, p = 0.002). A highly significantly-positive correlation was found between the regional inflammatory score and the length of time to full recovery (r2 = 0.92, p = 0.01, linear regession). A regional inflammatory score of 5 points with a sensitivity of 100% but a specificity of only 16% also identified patients at risk of complex regional pain syndrome. None of the biochemical parameters studied correlated with regional inflammatory score or predicted the development of complex regional pain syndrome. Our study suggests that patients with a distal radial fracture and a regional inflammatory score of 5 points or more at eight to nine weeks after injury should be considered for specific anti-inflammatory treatment.

Item does not contain fulltext OBJECTIVE: To investigate the effects of pentoxifylline (PTX) administration in a murine model for the multiple-organ dysfunction syndrome (MODS). DESIGN AND SETTING: Prospective double-blind randomized animal study in a university research laboratory. INTERVENTIONS AND MEASUREMENTS: Sixty C57BL/6 mice were given an aseptic intraperitoneal injection of lipopolysaccharide followed after 6 days by zymosan (day 0) at a dose of either 0.9 or 1.0 mg/g body weight. Starting on day 0 mice were administered PTX at a dose of 80 mg/kg body weight or saline per os every 8 h. On day 17 surviving animals were killed, and their liver, lungs, spleen, and kidneys were collected. RESULTS: Mortality, course of body temperature, body weight, and macroscopic lung damage were similar between zymosan-treated groups. Administration of PTX did not significantly alter survival, body temperature, body weight, or macroscopic lung damage. In addition, there were no significant differences in organ weights between mice that received PTX and mice that received PBS. Although PTX inhibited the lipopolysaccharide-induced increase in tumor necrosis factor alpha and interleukin 6 expression (but not interleukin 1beta expression) at both mRNA and protein level in a murine macrophage cell line, tumor necrosis factor alpha mRNA expression in the livers of PTX-treated mice was not significantly inhibited. CONCLUSIONS: The results reported here do not support the hypothesis that PTX improves outcome in zymosan-induced multiple-organ dysfunction in mice.

Multiple organ failure (MOF) can be induced by sterile intraperitoneal injection of zymosan in the rat. This results in a typical triphasic illness with maximal clinical signs at Days 2 and 12. In this model, superoxide production and lipid peroxidation closely correlate with the triphasic clinical illness. In the present experiment we studied the effect of albumin conjugated superoxide dismutase (SOD) and catalase (CAT) on lipid peroxidation and organ damage in the acute phase (Days 1 and 2). Lipid peroxidation in plasma was significantly decreased by SOD and CAT but clinical condition, mortality, and organ damage did not improve. We conclude that oxygen radical damage is not a key factor in the pathogenesis of the acute phase of multiple organ failure.

Multiple Organ Failure (MOF) has largely been attributed to bacterial sepsis, though conclusive evidence of an essential role for bacteria and/or their endotoxins is still lacking. On the other hand, MOF and the clinical syndrome of sepsis may be aseptically induced in germ-free animals. This paper reviews the evidence that excessive activation of endogenous humoral mediators and inflammatory cells may cause this highly lethal syndrome.

Our objective was to describe the characteristics of subareolar breast abscesses and to analyze the results of surgical treatment in relation to the prevention of recurrences. Almost 70% of patients smoked more than 10 cigarettes a day. The recurrence rate after excision of the lactiferous ducts was 28% and after management without excision of the lactiferous ducts was 79% (p < 0.001). Gram-positive bacteria were isolated more frequently in primary subareolar breast abscesses (not significant). Anaerobic microorganisms were more frequently cultured in recurring subareolar breast abscesses (p = 0.02). Definitive treatment of subareolar breast abscesses should consist of excision of the affected lactiferous ducts.

CRPS I is een ziekte die ernstige invaliderend kan zijn, niet alleen van het aangedane lidmaat maar van de gehele persoon. Vooropstaande problemen zijn het verlies aan kracht en uithoudingsvermogen, de stoornissen in de sensibiliteit en de sturing, overgevoeligheid voor koude en temperatuurwisselingen, en continu aanwezige pijn.

Traumatology in the Netherlands gained considerable momentum during the last years of the twentieth century. This breakthrough was due to the creation of ten trauma care centres, each with its own 'mobile medical team'. Additionally, four of these centres dispose of a helicopter for rapid transport of this team. Furthermore, within the field of medical education and training, new courses on advanced trauma and life support (ATLS) and advanced pediatric life support (APLS), for example, not only offer more practical knowledge, but also provide a 'common language' for all those involved in the medical and organisational aspects of trauma care. Surgical treatment of trauma injuries is becoming increasingly oriented towards minimally invasive techniques. Assessment of the quality of care provided requires a broad and reliable registration system for injuries.

Posttraumatische Dystrofie (pd) is een term die gebruikt wordt voor een tot op heden slecht begrepen reactie van een ledemaat op een trauma of operatie.

To survive in nature all animals, inducing humans, need an efficient defense system to overcome minor trauma and common infections. It had been observed as early as ancient times that limited damage to some part of the body can lead to the collapse of vital organ systems, remote from the original ate of impact. Fever and prostration were thought to be caused by “toxins” developing within the wounds. Since the discovery of their pathogenic potential, bacteria seemed to be always present in these cases, suggesting that infection is the decisive factor prohibiting recovery. When effective antimicrobial agents became available, it was originally expected that “killing the bugs” would put an end to disease in serious infections. It was soon experienced, however, that the initial physiologic derangement caused by trauma or infection may progress and kill the host, even when at autopsy no remaining infectious focus can be demonstrated.1

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Between 1993 and 1996 nine mentally retarded patients presented because of an acute abdomen. All had the habit of aerophagia, diagnosed previously by a general practitioner. Massive distension of the bowel led to ileus, volvulus, and necrosis. After placement of a percutaneous endoscopic gastrostomy catheter or performing a gastrostomy during laparotomy with the intention to use as a desufflator, no recurrence of the signs and symptoms of an acute abdomen were observed.

Since the introduction of a 10 point scale for newborn infants [1] in 1953 by Apgar numerous scores and scales have been developed in medicine. A score is an attempt to integrate many different information like blood pressure, heart rate or laboratory data into a single one-dimensional numerical value. The more complex a clinical situation is the more efforts are made to develop and refine score systems. Therefore, many scores for patients in the intensive care unit (ICU) have been published.

The effect of zymosan-induced generalized inflammation on the microcirculation of distant striated skin muscle was studied for a 12 day period in awake Syrian golden hamsters (n = 18) using the dorsal skinfold chamber model and intravital fluorescence microscopy. Intraperitoneal zymosan exposure (125 mg/100 g body weight) induced significant nutritive perfusion failure in the distant striated muscle tissue at Day 1 without complete recovery over the 12 day observation period, as indicated by the marked reduction of functional capillary density when compared with both baseline values and values of sham-treated control animals. Moreover, intraperitoneal zymosan exposure induced endothelial disintegration, as demonstrated by the continuous increase of macromolecular leakage throughout the 12 days of observation. Strikingly, zymosan did not induce significant leukocyte adherence to the endothelial lining of postcapillary and collecting venules of the striated muscle tissue. Thus, we conclude that in this model of generalized inflammation nutritive perfusion failure and loss of endothelial integrity in distant striated muscle is not mediated by activated leukocytes, but must rather be attributed to direct toxic effects of mediators, elicited by the local (intraperitoneal) zymosan challenge and systemically released.

A well defined animal model is a prerequisite to test intervention strategies aimed at preventing the development of the multiple organ dysfunction syndrome. This study compares changes in clinical parameters to histopathologic changes in tissues, observed over a 12 day period after a single intraperitoneal injection of zymosan in C57BL/6 mice. Administration of zymosan induced gradual and progressive changes in wet and dry organ weight of the liver, kidneys, and particularly, lungs and spleen that correlated with increasing histopathology. From 6 days after zymosan injection onwards, hemorrhagic spots were found in the lungs evolving into massive hemorrhages at 12 days, when thickened interstitial walls and loss of the honey comb-like structures were observed. The liver displayed progressive accumulation of macrophage-like and mononuclear cells. After 12 days, numerous granuloma-like structures were disseminated throughout the liver parenchyma. The spleen displayed great changes in red and white pulp with increasing numbers of megakaryocytes and plasma-like cells. In the kidneys, necrosis of the tubular epithelium adjacent to granulomas on the ventral (peritoneal) side was found. In mice, a single intraperitoneal challenge with zymosan leads to progressive multiple organ damage, which becomes apparent at some time after the insult. This animal model displays a number of features encountered in human multiple organ dysfunction syndrome and appears suitable to conduct intervention studies.

Sepsis associated with the sequential and progressive failure of multiple organs (MOF) presently is the major cause of death in surgical and ICU patients. The mortality from MOF still is around the 60%, despite optimal treatment and administration of a variety of antibiotic regimens. While by definition sepsis requires the causal involvement of bacteria, a clear, causal, exclusive, correlation between bacterial and/or (endo)toxin data and clinical data in patients with apparent sepsis/MOF has never been demonstrated [1, 2].

The in-hospital management of polytrauma patients can be divided into four periods [1]. In the acute period problems of the ABC (airway, breathing, circulation) are addressed. When vital functions have been stabilized, the primary period starts, with time for further diagnostic procedures and for a second series of operations, addressing injuries that may become life-threatening in the near future, or which may lead to severe disability if not treated early. The secondary period begins after 48–72 h, when the patient has been optimally stabilized. During the secondary period, operative reconstruction may be performed of major closed joint injuries (e.g., acetabular fractures) and closed fractures of the forearm. The tertiary period follows after 6–7 days and is determined by two events, septic complications and rehabilitation of the patient. Optimal rehabilitation can start after only operative stabilization of all major fractures, or consolidation of such fractures if treated conservatively.

To evaluate the posttraumatic course of several inflammatory mediators or markers (complement components C3, C3a, terminal complement complex, thromboxane B2, C-reactive protein, elastase, and neopterin) in relation to the development of multiple organ failure and mortality.Prospective study of a selected patient group.Surgical intensive care units in three European trauma hospitals.Patients (n = 56) with severe blunt trauma (Injury Severity Score ofor = 33).Arterial blood samples were sequentially obtained.Nonsurvivors (n = 8) had significantly higher circulating C3a and elastase concentrations on the first postinjury day, compared with survivors (n = 48). No differences between these groups were found for terminal complement complex, thromboxane B2, C-reactive protein, and the neopterin/creatinine ratio. Five patients died before day 5. Eighteen patients developed multiple organ failure, which was diagnosed from day 5 onward, leaving 33 patients without multiple organ failure. The patients with subsequent multiple organ failure showed significantly higher mean circulating concentrations of C3a (914 +/- 190 [SEM] ng/mL), terminal complement complex (57 +/- 17 U/mL), and thromboxane B2 (275 +/- 37 pg/mL) at the first postinjury day than the patients without multiple organ failure (566 +/- 110 ng/mL, 27 +/- 2 U/mL, and 169 +/- 14 pg/mL, respectively). In patients with multiple organ failure, elastase concentrations were significantly higher on days 2, 3, 4, and 5 postinjury. Neopterin/creatinine ratios, on the other hand, were significantly higher in patients with multiple organ failure when the multiple organ failure had already become established (on days 8 and 10).In multiple trauma patients, excessive triggering of the inflammatory cascade-as expressed by complement activation and stimulation of neutrophils producing elastase--plays an important and early role in the development of multiple organ failure.

The diagnostic workup of severely traumatized patients has evolved rapidly in recent years, with progressive integration of diagnostic and therapeutic procedures. This chapter addresses the clinical examination, additional diagnostic laboratory investigations, and imaging techniques used in evaluating severely traumatized patients.

Splanchnic ischemia, leading to intestinal mucosal damage, is thought to be common in patients after severe trauma. The adequacy of mucosal oxygenation can indirectly be determined by gastric intramucosal pH (pHi) measurement. We prospectively examined the posttraumatic gastric pHi values in 15 multiple trauma patients. In all patients gastric pHi was measured using a tonometer via the nasogastric route. A pHi value < or = 7.32 was used to differentiate between normal and low gastric pHi. Six hours after the injury four patients showed abnormally low pHi levels. Four other patients with normal initial pHi values exhibited low pHi values during one or more of the next measuring periods. Three of these eight patients developed major complications (two, ARDS) and two of them subsequently died. The seven remaining patients never had abnormal pHi levels and all patients had an uncomplicated recovery. Although intestinal ischemia was expected to be a common condition in multiple trauma patients, no consistent pattern of abnormal pHi measurements in the direct posttraumatic course could be discovered. No correlation was found between initial pHi values (at 6 hours) and ISS, shock, and lactic acidosis or APACHE II scores on admission. It is concluded that monitoring gastric pHi is useful in severely injured patients admitted to the ICU.

In 84 patients with an intracapsular hip fracture, early technetium-99m methylene diphosphonate (99mTc-MDP) scintimetry could be carried out preoperatively of in the case of conservative treatments within 72 h after injury. Fifty-four patients were available for a 3-year follow-up. The corrected uptake ratio showed a very high accuracy in predicting secondary dislocation, non-union (NU), delayed union (DU) or femoral head necrosis (FHN) and was far more reliable than the uncorrected uptake ratio. The predictive value of scintimetric follow-up at a 2- or 12-week interval could not reach the same accuracy of early scintimetry in predicting poor outcome. A comparison of follow-up scintimetry after conservative treatment and osteosynthesis showed that the major vascular injury to the femoral head is caused at the moment of the initial trauma and that no additional damage occurs perioperatively with closed reduction and fixation with a Dynamic Hip Screw device. Scintimetry is a useful tool in predicting poor outcome due to FHN and/or NU in the treatment of intracapsular hip fractures.

Forty-three elderly patients with an intracapsular hip fracture were selected for a prospective randomised trial comparing osteosynthesis (DHS) versus primary hemiarthroplasty (HA) with a 3-year follow-up. The duration of the operation and the perioperative blood loss were significantly shorter in DHS, but inadequate reduction and/or fixation led to serious problems in this group. Clinical morbidity was lower after DHS. No difference could be demonstrated in the mortality rates, fracture- or operation-related complications or the need for secondary intervention. Reintervention could be carried out without additional risk in both groups and did not lead to poor end results. Comparable results were obtained with both methods up to 24 months. At the 36-month follow-up, a significantly worse outcome could be demonstrated in the HA group. We conclude that osteosynthesis is justified as the primary treatment of displaced intracapsular hip fractures in elderly patients. Endoprosthetic replacement can be safely used in cases where osteosynthesis has failed.

Shock, sepsis, and multiple organ failure are syndromes complicating primary clinical conditions such as hemorrhage, major trauma, and severe bacterial infections. They presently are major causes of mortality and morbidity in clinical medicine, despite the fact that the primary causes can be treated well. Hemorrhagic shock is treated by stopping the bleeding and replacing lost blood-volume. Septic shock is treated by eradicating the septic focus, restoring and supporting the circulation, and killing the invading micro-organisms by appropriately chosen antibiotics. It should be expected, with such causal treatment, that homeostasis is re-established and that all patients are cured within hours.

Today multiple organ failure (MOF) represents the cause number one of death in a surgical intensive care unit (ICU). However, the basic pathophysiology of this Syndrome still remains to be elucidated [1], Hypotheses on the pathogenesis of MOF include “generalized inflammation” resulting from an excessive activation of endogenous inflammatory mediators and cells [2], and “the gut as the motor of MOF”, implicating the role of translocating gut bacteria and endotoxins triggering the septic State [3]. In this respect, alterations of intestinal permeability (IP) have been shown to be associated with translocation of intraluminally present toxic substances and micro-organisms. The role of splanchnic ischemia, inducing increased IP, has been stressed [4], while monitoring intestinal mucosal metabolism (e.g. by gastric intramucosal pH measurements) has been shown to provide for early prognostic information [5, 6], and for a guideline in therapy, thereby improving outcome in ICU patients [7].

• Gut bacteria have been incriminated as causing or contributing to generalized sepsis with multiple organ failure in severely ill patients, and selective decontamination of the gastrointestinal tract of Enterobacteriaceae has been claimed to decrease septic complications in these patients. We studied the effects of selective decontamination of the gastrointestinal tract on survival and organ function in an experimental model of sepsis with multiple organ failure. Wistar rats were inoculated intraperitoneally with zymosan and randomized into control or treatment groups (trimethoprim or streptomycin sulfate). Selective decontamination effectively prevented bacterial translocation of Enterobacteriaceae. However, only early mortality was decreased, and only so in the streptomycin-treated rats. Selective decontamination did not result in a significantly better condition of the surviving animals on day 12. ( Arch Surg. 1991;126:561-565)

Today, multiple organ failure (MOF) is the primary cause of death in a modern surgical department. Prevention of MOF and finding an adequate type of treatment —which we do not yet have — should thus be the first priority in surgery. In order to be able to prevent MOF property, a good understanding of the pathophysiology of the syndrome is necessary. A few principles therefore have to be outlined first: 1. The causes of MOF are the same as those that cause adult respiratory distress syndrome (ARDS). This is not a coincidence: respiratory failure (ARDS) is rather the first organ failure noticed clinically in MOF and can be easily diagnosed. 2. MOF and ARDS may be induced by bacterial and non bacterial stimuli. Nonbacterial stimuli include severe trauma, burns, pancreatitis, and protracted hemorrhagic or cardiogenic shock. Bacterial causes include peritonitis, bacterial sepsis, or septic shock. 3. MOF induced by bacterial sepsis is identical to MOF induced by primarily nonbacterial causes such as trauma [3], and no single study could reliably establish a relationship between bacteremia and/or plasma endotoxin levels and MOF in patients who were clinically septic. The common denominator of MOF in both situations is in fact an exaggerated response of inflammatory cells in the human body to such stimuli [3, 8].

The adult respiratory distress syndrome (ARDS) and subsequent sequential failure of multiple organ functions (MOF) in association with generalised sepsis, now accounts for the deaths of 60% of patients dying in an “up to date” surgical department or intensive care unit. As MOF was almost non-existent before ARDS-patients were ventilated mechanically -the start of the intensive care era- it seems that intensive care has created its own disease. In fact, the first authors to describe ARDS and its management by mechanical ventilation were also the first to report that these patients subsequently die of sepsis (Asbaugh and Petty 1972).

Background Chronic recurrent subareolar breast abscesses (SBAs) are a distinct entity of non-puerperal breast abscesses. They are located in the retroareolar or periareolar area and occur as a result of obstruction of the lactiferous ducts by squamous metaplasia. Unfamiliarity with this entity often leads to inadequate treatment, and recurrences frequently appear with extended fistulas. For this reason, the incidence of and the treatment for SBAs were analysed retrospectively. Methods In two clinics all patients with non-puerperal breast abscesses were analysed during a 6-year period. Results Some 98 patients were included (in the same period 35 patients were treated for puerperal breast abscesses). In 85 patients a total of 204 SBAs occurred (the largest study known). The remaining 13 patients had other non-puerperal breast abscesses such as cystic breast disease, inflammatory breast carcinoma and fat necrosis. If treatment of the SBA did not include excising the ductus lactiferus, the recurrence rate was 72 per cent. If the ductus lactiferus was excised, the recurrence rate was 37 per cent. Conclusion If a patient presents with a non-puerperal breast abscess in a subareolar location, the first diagnosis to consider should be (chronic recurrent) SBA. Smoking appears to be an important precipitating factor. In a recurrent SBA most frequently anaerobic micro-organisms are cultured. The primary treatment of SBA may comprise only incision and drainage. However, this should be followed by excision of the affected ductus lactiferus, including a part of the mamilla. If the affected ductus is not sufficiently excised, the SBA is destined to become a problematic chronic recurrent abscess.

Background Tumour necrosis factor (TNF) is believed to be a crucial mediator in systemic inflammation and the multiple organ dysfunction syndrome (MODS). Previous studies in this laboratory with a murine model have shown that interventions directed at TNF could mitigate the symptoms of zymosan-induced MODS. The present study aimed to investigate the course of MODS in the absence of TNF. Methods Twenty-four TNF/LT-knockout (−/−) mice and 25 wild-type (+/+) mice received an intraperitoneal dose of lipopolysaccharide 40 μg, followed by zymosan 1 mg per g body-weight 6 days later (day 0). Survival, body-weight and body temperature were monitored. At day 22 ten −/− mice and five +/+ mice were killed, and organs were collected and weighed. The remaining animals were followed until day 48, when all were killed and their organs harvested for histological examination. Results In all animals zymosan induced an acute sterile peritonitis phase followed by an apparent recovery. From day 8 onwards the +/+ mice entered a third, MODS-like, phase, characterized by loss of body-weight, decreased body temperature and significant mortality rate. At day 22, survival in the −/− mice was 92 per cent, which was significantly (P < 0·05) higher than that in the +/+ mice (60 per cent). In addition, mean body temperature and mean relative body-weight (versus weight at day 0) were 33·3°C and 84 per cent respectively in the +/+ mice. Data for the −/− mice were 35·9°C and 100 per cent respectively (P < 0·05). However, at this time point, both the +/+ mice and the −/− mice showed significant and similar organ damage, indicated by an increase in absolute and relative (versus body-weight) weight of lung, spleen and liver (the last organ only in the −/− mice). Moreover, at day 48 histopathological examination of liver, lungs, spleen and kidneys from the surviving animals showed a similar degree of microscopic damage in both the −/− and +/+ mice. Conclusion TNF-deficient mice exhibit significantly improved survival during zymosan-induced MODS and their clinical condition appears to be better than that of wild-type animals. However, surviving animals from both groups eventually display a similar degree of organ damage. Thus, in this murine model, the absence of TNF does not completely protect against MODS.

Growing awareness of problems arising from over-use of antimicrobial agents has led to attempts to develop policies or guidelines for rational treatment. To follow the effects of guidelines, the percentage of patients receiving anti-microbial drug therapy, acquired from patient records, has been a frequently used parameter. In this paper the Defined Daily Dose (DDD) per 100 bed-days has been used instead. This parameter can be calculated by converting the number of units of antimicrobials, delivered to individual wards, to defined daily doses per bed-day. This parameter determines the probability of treating a patient with a particular drug, based on pooled data. The DDD per 100 bed-days has been used to follow changes in prescribing habits arising from the acceptance of and adherence to guidelines over a period of 5 years in a University Hospital.

The data of all trauma fatalities occurring in 12 Dutch hospitals during a period of 1 year were reviewed for management errors and preventable deaths by a panel of five surgeons trained in trauma care. Management errors occurred in 38% of the fatalities. There was a significantly higher percentage of management errors in small general hospitals (72%) than in large general (29%) and in university hospitals (34%). A (possibly or definitely) preventable cause of death was identified in 25% of the fatalities. There was a significantly higher preventable cause of death rate in small general hospitals than in both other hospital categories. Of all fatalities, 21% were classified as preventable deaths. A significantly higher preventable death rate occurred in small general hospitals (48%), than in large general (14%) and university hospitals (19%). From these results, it can be concluded that management errors and preventable deaths are general phenomena occurring in any hospital. However, they occur significantly more frequently in hospitals not especially equipped to manage severely injured patients.

Summary A retrospective analysis was carried out on 89 patients who had died of blunt injuries. Death occurring more than 7 days after injury was caused by failure of a remote organ, associated with sepsis in 88 per cent of the cases. The only distinctive feature of the group dying from sepsis was a high average Hospital Trauma Index (HTI) for ‘limb injury’. Inadequate immobilization of major fractures in the multiply injured patient may be a contributory factor to late deaths from sepsis.

Multiple organ failure (MOF) was induced by sterile intraperitoneal inoculation of zymosan in the rat. This results in a typical triphasic illness with maximal clinical signs at Days 2 and 14. In this study, granulocyte superoxide production (unstimulated and phorbol myristic acid stimulated) was studied as well as lipid peroxidation (TBAR) in plasma, liver, and lung tissue. Mainly TBAR levels in liver and lung tissue closely correlated with the triphasic clinical illness, while bacteriological data did not. It is concluded that the severe inflammatory response in this experimental model probably is the result of excessive toxic oxygen radical production. The first phase of illness may mainly be due to oxygen radical formation by activated PMN, the third phase of illness to the production of lysosomal enzymes (proteinases) from PMN, and activated macrophages as indicated by elevated N-acetylglucosaminidase levels.

A combination of conservative measures was used to treat 105 patients with 119 ingrowing toenails. The method proved to be simple and cheap, but time consuming. Post-treatment discomfort and the time taken to return to normal activities were acceptable; the cosmetic result was good. Two-year follow-up revealed that the success rate of the method in less advanced cases (stages I and II) was high (96 per cent), although in the long term there was a tendency to recurrence in stage II cases. The failure rate in advanced cases (stage III) was high (up to 62 per cent). Conservative treatment can be used successfully in mild cases of ingrowing toenails.

Standards concerning the use and abuse of antibiotics have been carefully discussed and established (1). Similar standards should also be elaborated to improve the clinical use of albumin and plasma protein infusions. The extensive and careful investigations on albumin use, culminating in the Workshop on Albumin in 1975 (Workshop on Albumin, Feb. 12–13, 1975, National Heart and Lung Institute, National Institute of Health Bethesda Md, U.S.A.), already provided us with a number of guidelines. In this chapter I would like to discuss some standards gathering when or when not to use albumin infusion in acute clinical conditions and the saving of albumin that could have resulted—retrospectively—from the application of these standards in our patients.

Multiple-organ failure is generally attributed to bacterial infection, although a correlation with positive blood cultures is not consistently found. Consequently, we studied the effects of a local nonbacterial inflammatory stimulus on distant organ functions and metabolism. Wistar rats were inoculated intraperitoneally with zymosan. Heart and ventilatory rates, oxygen consumption, and body temperature were measured. Survivors were killed at day 12 for blood analysis, weighing of organs, and microscopy. Intraperitoneal zymosan resulted in an early hyperdynamic "septic" response with a 35% mortality. After a few days, oxygen consumption decreased, serum lactate levels increased, and the function of multiple organs deteriorated, while blood cultures remained sterile. The experiment was repeated in germ-free rats with similar results but a lower mortality. We concluded that a severe inflammatory response in itself is capable of inducing multiple-organ failure with "sepsis."

Sepsis and trauma are associated with the release of numerous mediators, which may contribute to cell injury in vital organs. The microcirculation is the primary target to undergo morphologic as well as functional changes. These alterations are caused by nonbacterial inflammation of the specific organ, which may represent a place of least resistance for additional bacterial infection. As a result, MOF (multiple organ failure syndrome) develops, and in many instances is fatal (Eiseman et al. 1977; Goris et al. 1985).

Presently adult respiratory distress syndrome (ARDS) and the subsequent syndrome with Multiple Organ Failure (MOF) and sepsis are the main causes of death in an up-to-date surgical and intensive care department. Despite intensive treatment, and support of the failing organ functions, mortality of the MOF syndrome still is around 60%. MOF is generally believed to be the result of bacterial sepsis, though it has been recently shown that — at least in trauma patients — no dependable correlation is present between positive bacterial blood cultures and “sepsis” [1].

During the first 48 hours after a severe burn, the main clinical problem is development of burn shock. Patients are treated according to different protocols (Evans et al., 1952; Moore, 1970; Monafo et al., 1973). Large amounts of isotonic or hypertonic saline and/or colloids are administered. Diuresis is used as a parameter to control the infusion rate.