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Background: The number of burn patients over the age of 75 receiving advanced treatment, including extensive surgery and intensive care, is increasing. We aimed to describe the treatment and outcomes for burn patients over the age of 75 admitted to the National Burn Centre at Haukeland University Hospital. We also wanted to investigate whether frailty scores can be a predictor of the treatment outcome., Material and Method: All patients ≥ 75 years admitted to the National Burn Centre at Haukeland University Hospital in the period 2000-19 were included in the study. Frailty scores were calculated retrospectively based on patients' medical records., Results: Our study included 101 patients (50 women and 51 men). The number of admissions of older burn patients increased from an average of 3.3 per year in 2000-14 to 10.2 in the period 2015-19. The median total body surface area with burns was 11 % (range 0.9-80 %). Seventeen patients received palliative care, and 12 patients receiving active treatment died in hospital. In 68 of 84 (81 %) actively treated patients, tangential excision and split-thickness skin grafting were performed. The remainder received conservative treatment (non-surgical) with wound care and application of a silver dressing. Patients who died in hospital had a significantly higher total body surface area with burns (p < 0.0001) and higher frailty scores (p = 0.003) than patients who survived., Interpretation: The yearly number of patients over the age of 75 treated at the National Burn Centre tripled during the period. More than two-thirds of the patients were discharged alive. Extent of burn injury and frailty score are associated with mortality and may be useful for adjusting therapy.

Background: According to current guidelines, initial burn resuscitation should be performed with fluids alone. The aims of the study were to review the frequency of use of vasoactive and/or inotropic drugs in initial burn resuscitation, and assess the benefits and harms of adding such drugs to fluids., Methods: A systematic literature search was conducted in PubMed, Embase, Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, UpToDate, and SveMed+ through 3 December 2021. The search included studies on critically ill burn patients receiving vasoactive and/or inotropic drugs in addition to fluids within 48 h after burn injury., Results: The literature search identified 1058 unique publications that were screened for inclusion. After assessing 115 publications in full text, only two retrospective cohort studies were included. One study found that 16 out of 52 (31%) patients received vasopressor(s). Factors associated with vasopressor use were increasing age, burn depth, and % total body surface area (TBSA) burnt. Another study observed that 20 out of 111 (18%) patients received vasopressor(s). Vasopressor use was associated with increasing age, Baux score, and %TBSA burnt in addition to more frequent dialysis treatment and increased mortality. Study quality assessed by the Newcastle-Ottawa quality assessment scale was considered good in one study, but uncertain due to limited description of methods in the other., Conclusion: This systematic review revealed that there is a lack of evidence regarding the benefits and harms of using vasoactive and/or inotropic drugs in addition to fluids during early resuscitation of patients with major burns., (© 2022 The Authors. Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.)

Background: It is unknown whether lung-protective ventilation is applied in burn patients and whether they benefit from it. This study aimed to determine ventilation practices in burn intensive care units (ICUs) and investigate the association between lung-protective ventilation and the number of ventilator-free days and alive at day 28 (VFD-28)., Methods: This is an international prospective observational cohort study including adult burn patients requiring mechanical ventilation. Low tidal volume ( V T ) was defined as V T  ≤ 8 mL/kg predicted body weight (PBW). Levels of positive end-expiratory pressure (PEEP) and maximum airway pressures were collected. The association between V T and VFD-28 was analyzed using a competing risk model. Ventilation settings were presented for all patients, focusing on the first day of ventilation. We also compared ventilation settings between patients with and without inhalation trauma., Results: A total of 160 patients from 28 ICUs in 16 countries were included. Low V T was used in 74% of patients, median V T size was 7.3 [interquartile range (IQR) 6.2-8.3] mL/kg PBW and did not differ between patients with and without inhalation trauma ( p  = 0.58). Median VFD-28 was 17 (IQR 0-26), without a difference between ventilation with low or high V T ( p  = 0.98). All patients were ventilated with PEEP levels ≥5 cmH 2 O; 80% of patients had maximum airway pressures <30 cmH 2 O., Conclusion: In this international cohort study we found that lung-protective ventilation is used in the majority of burn patients, irrespective of the presence of inhalation trauma. Use of low V T was not associated with a reduction in VFD-28., Trial Registration: Clinicaltrials.gov NCT02312869. Date of registration: 9 December 2014., (© The Author(s) 2021. Published by Oxford University Press.)

Background: The objective of this article is to elucidate the scope of burn injuries in Norway, on the basis of those patients who had sustained a burn injury that caused hospitalisation through a calendar year., Material and Method: The article is based on data retrieved from the Norwegian Patient Registry on patients discharged from Norwegian hospitals in 2012 with a burn injury as their main diagnosis, supplemented with activity data for children admitted to the Burn Unit, Haukeland University Hospital, Bergen, during the period 2013 – 15., Results: In 2012, altogether 620 people (12.4/100 000 inhabitants) were hospitalised with burn injuries. Of these patients, 393 (63.4 %) were men. A total of 375 patients (60 %) were hospitalised more than once, and 124 (20 %) were admitted to more than one hospital. Altogether 367 patients (59 %) were hospitalised for less than eight days. Average hospitalisation time for the group as a whole was 11.3 days (SD 18.8 days). Many of the burn-injured patients were young: the average age was 27.4 years (SD 26.0 years). As many as 183 patients (30 %) were less than three years old. Children in this age group were admitted for burn injuries 12 times more frequently than children ≥ 5 years and adults., Interpretation: We found no definite reduction in burn injuries as a cause for admission to Norwegian hospitals in 2012 when compared to results from previous studies for the period 1992 – 2007. There ought to be a major potential for more effective prevention of burn injuries in the age group < 3 years, in which scalding (78 %) and contact with hot surfaces (most often stoves) (17 %) are the main mechanisms of injury.

Objectives: To study the incidence and outcome of burns in Norway in 2007, and to establish estimates for effective length of stay, mortality and economical costs., Methods: Data from the Norwegian Patient Registry on all patients discharged from all somatic hospitals in Norway in 2007 with main or subsidiary diagnosis of burn injury (ICD-10: T20-31) were collected., Results: Seven hundred and twenty-six patients (65.0% male) with acute burns were admitted to Norwegian hospitals in 2007, requiring 8157 in-hospital days and resulting in a mean length of hospitalization per burn case of 11.3 days (S.D. 15.2). The mean age of the patients was 26.9 years (S.D. 25.5), and the mortality was 2.1%. For children below 5 years of age the incidence of burns admitted to hospital was 82.5/100,000/year. The annual total cost for in-hospital burn care exceeded 10.5 million euros (2,200,000 euros/million inhabitants), Conclusion: Compared to similar data from Norway (1992) the rate of admission for burns in 2007 (15.5/100,000/year) appeared as high as in 1992, whereas the mean length of stay was reduced by 26%. Children under the age of 5 had a seven times higher incidence compared the rest of the population.

This study investigated the long-term mortality in 1182 burn patients admitted at a single burn centre in 1984-2003. One thousand and forty-nine patients were discharged alive, of which 999 (95.2% of all discharged) were available for follow-up (mean observation time: 9.6+/-5.5 (S.D.) years). One hundred and twenty-two patients had died after discharge but before follow-up. For 111 patients, the official information recorded from their death certificates revealed that 83 patients (mainly in the higher age groups) had died due to a variety of natural causes. Twenty-three patients (M:F=18:5) (age: 37.7+/-11.3 years), previously hospitalised for burns, had later suffered accidental or violent deaths, including suicide (5), assault (2), and deaths related to substance and/or alcohol abuse (12). Additionally, five other deaths were recorded as sudden death, with no additional specific information as to the cause of death. This study shows that the rates of accidental or violent death in previously burned adult patients (around 40 deaths per 1000 years at risk) may be an order of magnitude higher than that in the average Norwegian population.

Objective: To describe how surface cooling influences fluid distribution, vascular capacity and haemodynamic variables., Methods: Seven anaesthetised pigs, following normothermic stabilization for 60 min, were cooled to 27.8+/-1.6 degrees C. Fluid balance, haemodynamics, colloid osmotic pressures (plasma/interstitial fluid), haematocrit [s-albumin/protein] were recorded and plasma volume measured together with tissue perfusion during normothermia, cooling and stable hypothermia (coloured microspheres). Fluid shifts and changes in albumin and protein masses were calculated. At the end tissue water content was assessed., Results: Haemodynamic variables changed with the start of cooling in parallel with a decreasing cardiac output. During hypothermia the haematocrit increased from 0.31+/-0.01 to 0.35+/-0.01 (P < 0.01). Plasma volume decreased from 1139.0+/-65.4 ml at start of cooling to 882.0+/-67.5 ml 3 h later (P < 0.05). In parallel the plasma albumin and protein masses decreased from 37.8+/-2.5 g and 54.6+/-4.0 g to 28.0+/-2.7 g (P < 0.05) and 41.2+/-4.1 g (P > 0.05), respectively. The main changes occurred 120-180 min after start of each experiment. In this period the fluid extravasation rate was elevated (P < 0.05) without influencing the colloid osmotic pressure of plasma/interstitial fluid. The increased fluid filtration was reflected by an increase in tissue water content., Conclusion: Our results are in favour of a shift of plasma from circulation to the interstitial space during surface cooling. This conclusion is based on the parallel losses of fluid and proteins from circulation with unchanged colloid osmotic pressures (plasma/interstitial fluid). Inflammation may be involved.

Introduction: The incidence and outcome of acute respiratory failure (ARF) depend on dysfunction in other organs. As a result, reported mortality in patients with ARF is derived from a mixed group of patients with different degrees of multiorgan failure. The main goal of the present study was to investigate patient outcome in single organ ARF., Patients and Method: From 1 January 2000 to 1 July 2002, all adult patients (>16 years) in the intensive care unit (ICU) at Haukeland University Hospital were scored daily using the Sequential Organ Failure Assessment (SOFA) score for organ failure. ARF was defined by the SOFA criteria: ratio of arterial oxygen tension to fractional inspired oxygen, with a value < 26.6 kPa (200 mmHg) in more than one recording during the ICU stay (SOFA score 3 or 4). Patients with ARF alone and in combination with other severe organ failure (SOFA score 3 or 4) were included. Survival was recorded on discharge from the ICU, at hospital discharge and at 90 days after ICU discharge., Results: During the period of study, 832 adult patients were treated and 529 (63.0%) had ARF. The ICU, hospital and 3-month mortality rates were lowest in single organ ARF (3.2, 14.7 and 21.8%, respectively), with increasing mortality with each additional organ failure. When ARF occurred with four or five additional organ failures, the 3-month mortality rate was 75%. No significant differences in mortality were found between early and late ARF., Conclusion: The prognosis for ICU patients with single organ ARF is good, both in the short and long terms. The high overall mortality rate observed is caused by dysfunction in other organs.

Small volumes of hyperosmolar saline solutions may rapidly improve MAP and CO in hemorrhagic shock. In the present study, the effects of infusion of 7% NaCl on interstitial fluid volume and intracellular fluid volume were determined. In anesthetized, normovolemic rats either 7% NaCl (1.1 mL/100 g, intravenously), acetated Ringer's solution (10 mL/100 g), or no fluid (controls) were infused and extracellular volume (ECV) and plasma volume were determined in samples from skin, skeletal muscle, small intestine, liver, and lung. Intracellular volume was determined as local tissue water content minus ECV. Extracellular fluid volumes were 21.1 +/- .6 mL/ 100 g(mean +/- SEM; n = 6) (control animals), 26.1 +/- .4 mL/100 g (following 7% NaCl) (p < .05), and 32.8 +/- .5 mL/100 g (following Ringer's) (p < .05). Following 7% NaCl ECV increased by four to five times the infused volume. With 7% NaCl ECV in skin, muscle and intestine increased significantly, whereas cell volume was reduced by 10% in muscle and liver. Skeletal muscle, constituting > 40% of body mass with a large cell volume, was the main source for fluid mobilized by administration of 7% NaCl.

Hyaluronan (HYA) is an ubiquitous polysaccharide in connective tissue interstitium; its normal plasma concentration is in the nanogram/ml range. Following major burn injury in sheep, plasma HYA can increase to levels tenfold greater than normal. The present study aimed to determine the effects of major cutaneous burns on plasma HYA concentration in rat, since in this species, the HYA elimination kinetics may better resemble those in man. Thermal injury did not alter the weight-average molecular weight of HYA in skin. HYA concentration in plasma was 46 +/- 4 ng/ml (mean +/- SEM) in controls. Three hours after scald burns to 40% of the body surface area, plasma HYA was 61 +/- 10 ng/ml in unresuscitated animals (P less than 0.1 vs. controls). After fluid replacement by lactated Ringer's plasma HYA was 75 +/- 8 ng/ml (P less than 0.01 vs. control), whereas plasma infusion prevented the elevation of plasma HYA. HYA also increased significantly after lactated Ringer's infusion in noninjured animals. The increased plasma concentration of HYA after major burns is probably a consequence of increased lymph flow, increasing its transport from skin interstitium. Possibly, plasma concentrations of connective tissue components may be used as indicators of the severity and extent of burn injuries.

One of the obvious acute features of cutaneous thermal injury is the swelling of the involved tissue. This swelling is caused by a fluid shift from circulating plasma. Along with the evolution of intravenous fluid therapy in trauma and surgery, the implementation of such therapy to burn victims has improved survival. Edema generation aggravated by fluid therapy may, however, represent a source of increased morbidity. This paper presents a review of the literature on postburn edema generation, focusing mainly on fluid physiology. It is well documented that fluid is lost from the circulation into burned tissue because of a moderate increase in capillary permeability to fluid and macromolecules and a modest increase in hydrostatic pressure inside the perfusing microvessels. Recently it was discovered that a very negative interstitial pressure develops in thermally injured skin. This pressure constitutes a strong "suction" adding markedly to the edema generating effect of increased capillary permeability and pressure.

The present work is a continuation of studies concerned with mathematical modelling and simulation of microvascular fluid and protein exchange following burn injuries [Bert et al.: Circulatory Shock 28: 199-219, 1989: Bowen et al.: Circulatory Shock 28: 221-233, 1989]. The model has been extended to include the effects of different types of fluid resuscitation on the circulatory and microvascular exchange systems. The model and a statistical fitting procedure were used to find the ranges of fitting parameter values that best describe the changes in interstitial fluid volume and protein mass as well as transcapillary protein extravasation for three sets of experiments (no resuscitation, resuscitation with Ringer's or resuscitation with plasma). Typical changes in mass exchange related parameters postburn that resulted in simulation predictions which were a good fit to the experimental data include: an increase in the large pore pathway for protein of 100 times in the injured skin and 5 times in non-injured skin and skeletal muscle, an increase in fluid filtration coefficients in injured skin of 10 times and an instantaneous decrease of 50% in the area available for exchange in injured skin at the time of the burn.

Hyaluronan (HYA) is an important structural element in skin and is presumably participating in regulation of the interstitial fluid volume. HYA is transported via the lymphatics from the tissues to the blood, where its concentration is normally very low. Fluid flux through the interstitium is markedly increased after thermal injury. The present study was performed to determine whether major thermal injury would affect plasma levels of HYA. In halothane-anesthetized sheep subjected to 40% BSA full-thickness scald burns, plasma HYA concentration increased from 116 +/- 19 (mean +/- SEM) to 172 +/- 18 ng/ml within 1 hr after injury (P less than 0.05). After 3 hr of fluid therapy plasma HYA concentration was further elevated to 10 times baseline (1417 +/- 322 ng/ml) (P less than 0.01). To clarify whether this rise represented an increased "washout" of interstitial HYA, attributable either to the burn injury or the subsequent fluid therapy, awake sheep were subjected to overhydration. Following a 3-hr infusion of lactated Ringer's 2.5 liter/hr, plasma HYA concentration increased to 2-3 times baseline. Lung lymph flow and its concentration of HYA increased, leading to an increase in the lymphatic flux of HYA to 10-20 times baseline. In peripheral lymph HYA flux increased 2-3 times baseline. Infusion of lactated Ringer's markedly increased lymphatic removal of HYA. However, plasma concentrations of HYA were 3 times higher after thermal injury than following fluid challenge alone, suggesting that thermal injury per se may also increase input of HYA into the systemic circulation.

The effects of fluid therapy on interstitial colloid osmotic and hydrostatic pressures in thermally injured skin were investigated in anesthetized rats subjected to full-thickness scald burns to 40% of the body surface area and resuscitation for 3 hr by either lactated Ringer's or plasma. Interstitial fluid hydrostatic pressure (Pif) was reduced from -2 mm Hg to -20 to -40 mm Hg after injury, which will profoundly increase transcapillary filtration. Following the onset of fluid therapy, Pif increased to slightly positive values. In control, colloid osmotic pressure in plasma (COPp) was 20.6 +/- 0.4 mm Hg and in interstitial fluid (COPif) 13.7 +/- 0.3 mm Hg (means +/- SEM). The transcapillary oncotic pressure gradient (COPgrad = COPp-COPif) was 6.9 +/- 0.4 mm Hg. Following nonresuscitated thermal injury, COPp declined to 18-19 mm Hg (P less than 0.05) and COPif was reduced to 10.4 +/- 0.5 mm Hg (P less than 0.05). Fluid therapy by lactated Ringer's markedly reduced COPp (12.3 +/- 0.3 mm Hg; P less than 0.05), and COPgrad was almost abolished (2.6 +/- 0.7 mm Hg; P less than 0.05). In contrast, plasma infusion maintained COPp, whereas COPgrad increased significantly (11.1 +/- 1.2 mm Hg; P less than 0.05). Noncolloid saline solutions have been preferred for the initial fluid therapy for burns. The present study provides evidence that this will reduce both COPp and COPgrad, a situation in which edema formation will be favored.

Hyaluronan (formerly hyaluronic acid) is an important constituent of the interstitial matrix in skin. Following major burn injury in animal models, plasma hyaluronan can increase to levels 10-fold greater than normal. The present experiments were designed to determine whether this is a result of the increased lymph flow (QL) accompanying the injury or of an increased release of hyaluronan from the burned skin and subcutaneous tissue. The lateral saphenous vein and a prenodal lymphatic were cannulated in the hindpaw of five anesthetized canines. Hindpaw venous pressure was elevated until the total protein concentration in lymph declined to steady-state levels, and QL and hyaluronan flux (QL X [hyaluronan]) was measured. A minor burn was inflicted by immersion of the paw into 100 degrees C water for five sec, and measurements were repeated at regular intervals for a minimum of 4 hr. Burn injury resulted in significant and persistent increases in QL (154 +/- 61 microliters/min versus 562 +/- 105 microliters/min 4 hr postburn) and lymph total protein concentration (1.34 +/- 0.04 g/dl versus 4.08 +/- 0.18 g/dl 4 hr postburn), while lymph hyaluronan concentration fell (3.01 +/- 0.20 micrograms/ml versus 2.1 +/- 0.16 micrograms/ml 4 hr postburn). The resultant increase in hyaluronan flux (0.42 +/- 0.13 microgram/min versus 1.17 +/- 0.22 microgram/min 4 hr postburn) appears to be a function of lymph flow rather than burn-induced release of skin hyaluronan. Hence, the increased plasma concentration of hyaluronan following major burns is likely a consequence of increased lymph flow from the site of injury.

Small-volume resuscitation (4 ml/kg) with hypertonic saline-dextran (HSD) has been shown effective in hemorrhagic shock. In the present study the effectiveness of an initial 4 ml/kg bolus infusion of HSD on cardiovascular function and fluid resuscitation requirements after a major burn injury was evaluated in anesthetized sheep following a 40% BSA scald burn. One hour after injury resuscitation was initiated by a rapid intravenous bolus infusion (4 ml/kg) of either hypertonic saline-dextran (7.5% NaCl in 6% dextran 70) (HSD) or the same volume of normal (isotonic) saline (NS). Lactated Ringer's was later infused as needed to maintain cardiac output at 90% of baseline. HSD rapidly and effectively restored cardiac output and mean arterial pressure significantly better than the same volume of NS. Hemodynamic improvement by HSD was short lived, and need for further fluid therapy was only marginally delayed (HSD 38 +/- 8 min, NS 20 +/- 3 min; p = 0.06) (mean +/- SEM). The total requirements for fluid therapy during the first 6 hr postburn were not reduced by the initial HSD bolus (HSD 3,145 +/- 605 ml, NS 2,905 +/- 495 ml; n.s.), nor was skin edema formation reduced. We conclude that in anesthetized sheep HSD resuscitation was only transiently effective in treating burn shock. This may be attributed to the sustained increase in vascular permeability and continued plasma leak following thermal injury.

Pentobarbital anesthetized rats were subjected to a 40% body surface area full-thickness scald burn. Intravenous fluid therapy was given as lactated Ringer's (5 ml/hr), plasma (2.5 ml/hr), or very hypertonic saline (2,400 mosmol/l) (0.75 ml/hr) and compared to unburned or burned, untreated controls. At 3 hr postburn, skin water and albumin content and extravasation of radiolabelled albumin were determined. Water content in injured skin increased by 35-78% (least in the untreated group, most in the plasma group) compared to unburned controls (P less than 0.05). After lactated Ringer's therapy water content increased even in unburned skin and in muscle (P less than 0.05). Tissue albumin mass increased generally slightly more than the increase in water content, from 37% (lactated Ringer's group) to 126% (plasma group) in burned areas. Extravasation rate of radiolabelled albumin increased 5-80 times in burned areas, most following plasma treatment (equivalent to 0.6-1.0 ml plasma/g dry weight/180 min). A major part of the estimated total fluid loss following therapy by lactated Ringer's took place in noninjured tissue. Plasma therapy gave less fluid accumulation in unburned tissues but more edema in the injured areas than lactated Ringer's.

We have measured tissue pressures in excised rat skin subjected to in vitro burn injury and investigated the mechanisms behind the increased imbibition (swelling) pressure in burned skin. Skin pieces wrapped in aluminum paper were immersed into boiling hot water for 10, 30, or 60 s. Dermal imbibition pressure was measured with micropipettes and tissue osmometry as interstitial fluid hydrostatic pressure (Pif) and/or interstitial fluid colloid osmotic pressure (COPif). COPif was also measured in interstitial fluid sampled with intradermal wicks. Control values of Pif (micropipettes) and of COPif (wick fluid) averaged -1.5 mmHg and -17.5 mmHg, respectively. An increase in imbibition pressure was seen after thermal injury. After 10 s of heat exposure, the imbibition pressure gain was mainly due to a strongly negative hydrostatic pressure (Pif mean value -33.3 mmHg). Pif became slightly positive and COPif increasingly negative after longer exposure (mean Pif 0.3 and mean COPif -133 mmHg after 60-s exposure). Collagen degradation and water solubility increased with extension of the heat exposure time. Thermal degradation of collagen seems to be the main mechanism responsible for the generation of increased imbibition pressure.

Heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), and cardiac index (CI) were measured in anesthetized rats subjected to a 40% body surface area full-thickness scald burn. Postburn intravenous fluid therapy with lactated Ringer's (5 ml/hr), plasma (2.5 ml/hr), or very hypertonic saline (2,400 mosmol/l) (0.75 ml/hr) was compared to unburned or burned, untreated controls. HR and CVP were not influenced significantly by thermal injury. MAP decreased steadily in the untreated group from 110 mmHg to 80 mmHg at 3 hr postburn. In the fluid-treated groups MAP did not change significantly. During the first 15 min postburn, CI was reduced to 58-71% of control values (P less than 0.01). CI increased during Ringer's and plasma infusion to 74-80% of control values (P less than 0.02 vs. unburned). Despite infusion therapy, hematocrit increased from 48 to 52%, clearly less than in the unresuscitated group (increase from 48 to 58%). Theoretically, the 2,400 mosmol/l saline would expand extracellular volume by five to six times the infused volume. Still, CI was reduced by 55% at 3 hr postburn in the hypertonic saline as well as in the burned, untreated group (P less than 0.001 vs. unburned). The low CI was mainly due to a reduced stroke volume.

In a prospective double-blind trial, low molecular weight (LMW) heparin (KABI 2165) 5,000 U (anti-Xa) once daily was compared with conventional heparin 5,000 IU twice daily, both given subcutaneously, as regards prevention of postoperative deep venous thrombosis (DVT) in 52 patients undergoing major abdominal surgery. Radioactive fibrinogen uptake test (FUT) was used for DVT screening. DVT, diagnosed from positive FUT, developed in two patients from each group, but could be phlebographically confirmed in only one (LMW) case. No intergroup differences were found in peroperative blood loss or requirements for blood transfusion. Complications attributable to the prophylactic regimens were few. In the LMW-heparin group, the anti-Xa levels measured during operation showed considerable variation, the higher activities (greater than 0.30 U/ml) being nonsignificantly associated with increased blood loss. Studies with lower doses of LMW-heparin are recommended.