Hypertonic saline

[hammerpcp]

Is anyone using hypertonic saline in the field? What do ou think about it so far? Does anyone know by what mechanism it can cause seizure?

[Nate]

No, we don't have that.

[medik8]

We don't use it, and therefore I can't give an educated answer to your question. I know that depending on how it's given, it has the possibility to cause intracranial pressure, as well as elevated BP, HR, and RR. And of course, little facts like rapid correction of hyponatremia with hypertonic solution = myelinosis =yikes... :shock:

[AZCEP]

Is anyone using hypertonic saline in the field? What do ou think about it so far? Does anyone know by what mechanism it can cause seizure?

Don't have it, yet. Not really sure that it would be worth having, yet either.

As for the seizure concern, anytime you dump a large amount of electrolyte into the blood, you can cause rapid fluid shifts out of the neural cells, making them hyperresponsive and thus cause a seizure.

Give it a while, and I'm sure the Doc's(Zilla & ER) will chime in.

[Ridryder 911]

I have not seen "hot saline" used in the field as of yet. Although, there are many indications, I would be very cautious of using any without a base line CMP.

Be safe,

R/R 911

[akroeze]

ACPs in Lambton county here in Ontario are going to be in a study of its use is what I'm told.

[ERDoc]

Hypertonic saline is generally 3% (though other concentrations do exist), compared to 0.9% for NS. Giving too much can do very bad things. If you increase the osmolarity in the blood too high, you draw fluid out of the brain space, causing major shrinkage (JK), but you do get a major fluid shift out of the brain that can lead to seizures. As someone else said, if you correct hyponatremia too quickly you can get central pontine myelinolysis (bad). The only uses for hypertonic saline that I can think of would be to correct hyponatremia, but I can't see you doing this in the field since you will not be able to get a sodium level. In this case it is used as a slow drip. In seizures secondary to hyponatremia you give it as a bolus, but it is not like giving a NS bolus, give a liter and you could kill (bad, again) by the means I mentioned before. Unless you get some sort of method for checking sodium in the field, I really don't think there is much need for hypertonic saline.

[hammerpcp]

The hypertonic saline is a reserch study that is going to be done in association with ambulance services all over north america, in the near futre. Apparently its use has already been extensilvey studyed in the military. I believe it will be 7.5%. In this study 250ml will be rapidly infused into pts with hypovolemia or head injury. there are other vital sign indications but i don't remeber what they are. Anyway i was jus curious if anyone out there had had any experience with this before. very interesting.

[Doczilla]

I agree with ER Doc here. Even in-hospital there is little call for "hot salt". I've only seen it once- today- on a patient with a sodium of 105, which is often incompatible with life. Even in the moderately hyponatremic patient, boluses of NS are used to correct the sodium level.

Some in the special operations community will use it as a volume expander in trauma patients when it is not possible to carry large volumes of fluid. The idea is that the added sodium will draw water into the vasculature by the osmotic pressure, thereby getting you a lot of mileage with a small amount of fluid in your pack. This might be okay, but it makes a lot of assumptions: a) the patient is young and healthy and does not have a derangement of sodium already, they don't have kidney or serious heart disease, 3) they aren't already dehydrated (and possibly hypernatremic), which may be a stretch in a soldier who has been on the battlefield in body armor for hours already. I'd probably reach for the hespan before the hypertonic saline in this situation.

Note, though, that the colloidal solutions (hespan) and hypertonic saline haven't shown any benefit in trauma patients over traditional isotonic fluids, so we stick to NS and LR when space and weight aren't an issue. This sounds like an interesting study.

'zilla

[Ace844]

(Received for publication May 16 @ 2005. Revision received July 11, 2005. Revision received August 6, 2005. Accepted for publication August 6, 2005

[u)

Hypertonic Lactated Saline Resuscitation Reduces the Risk of Abdominal Compartment Syndrome in Severely Burned Patients

[Original Articles]

Oda, Jun MD; Ueyama, Masashi MD; Yamashita, Katsuyuki MD; Inoue, Takuya MD; Noborio, Mitsuhiro MD; Ode, Yasumasa MD; Aoki, Yoshiki MD; Sugimoto, Hisashi MD

From the Department of Trauma, Critical Care Medicine, and Burn Center (J.O., M.U., K.Y., T.I., M.N., Y.O., Y.A.), Social Insurance Chukyo Hospital, Nagoya; and Department of Traumatology (H.S.), Osaka University, Osaka, Japan.

Submitted for publication September 20, 2005.

Accepted for publication November 22, 2005.

Presented at the 64th Annual Meeting of American Association for the Surgery of Trauma, September 22–24, 2005, Atlanta, Georgia.

Address for reprints: Jun Oda, MD, Social Insurance Chukyo Hospital, 1–1-10 Sanjo, Minami-ku, Nagoya, Aichi 457-8510, Japan; email: junoda@v001.vaio.ne.jp.

]

Abstract

Background: Secondary abdominal compartment syndrome is a lethal complication after resuscitation from burn shock. Hypertonic lactated saline (HLS) infusion reduces early fluid requirements in burn shock, but the effects of HLS on intraabdominal pressure have not been clarified.

Methods: Patients admitted to our burn unit between 2002 and 2004 with burns >=40% of the total body surface area without severe inhalation injury were entered into a fluid resuscitation protocol using HLS (n = 14) or lactated Ringer’s solution (n = 22). Urine output was monitored hourly with a goal of 0.5 to 1.0 mL/kg per hour. Hemodynamic parameters, blood gas analysis, intrabladder pressure as an indicator of intraabdominal pressure (IAP), and the peak inspiratory pressure were recorded. Pulmonary compliance and the abdominal perfusion pressure were also calculated.

Results: In the HLS group, the amount of intravenous fluid volume needed to maintain adequate urine output was less at 3.1 ± 0.9 versus 5.2 ± 1.2 mL/24 h per kg per percentage of total body surface area, and the peak IAP and peak inspiratory pressure at 24 hours after injury were significantly lower than those in the lactated Ringer’s group. Two of 14 patients (14%) in the HLS group and 11 of 22 patients (50%) developed IAH within 20.8 ± 7.2 hours after injury.

Conclusion: In patients with severe burn injury, a large intravenous fluid volume decreases abdominal perfusion during the resuscitative period because of increased IAP. Our data suggest that HLS resuscitation could reduce the risk of secondary abdominal compartment syndrome with lower fluid load in burn shock patients.

Abdominal compartment syndrome (ACS) can become fatal, because the acute elevation of the intraabdominal pressure (IAP) causes a syndrome consisting of multiple organ dysfunction characterized by decreased cardiac output, pulmonary dysfunction, splanchnic ischemia, elevated intracranial pressure, and acute renal failure if intraabdominal hypertension (IAH) is not appropriately treated. Secondary ACS is a lethal complication after resuscitation from burn shock because of massive resuscitation fluid and fluid shift. For ACS in burned patients, several case reports,1–4 changes of physiologic parameters by decompression,5,6 and a correlation between their IAP and total fluid volume 7 have been reported. Although the release of abdominal hypertension improves physiological parameters, including hemodynamics, abdominal perfusion,5 and survival 8 with burn injury, the general prognosis of ACS in burn patients is still poor.

The most important factor responsible for the development of ACS might be excessive fluid administration,5,7 which can shift to the third space because of increased capillary permeability. Treatment with hypertonic saline solution (HLS) has been well known since the 1970s for burn shock, and many investigators reported beneficial effects of HLS on reducing the amount of fluid administered for burn shock to maintain adequate circulatory volume and avoid volume overload after the resuscitation period.9–11 In the present study, we hypothesized that HLS resuscitation can reduce the risk of secondary ACS with lower fluid load in burn shock compared with resuscitation by lactated Ringer’s (LR) solution. We also compared parameters including abdominal perfusion, pulmonary function, and oxygenation between groups treated by resuscitation with HLS and LR solution.

PATIENTS AND METHODS

Approval for this study was obtained from the Chukyo Hospital Investigational Review Board. Between 2002 and 2004, 48 consecutive patients were admitted to our Burn Unit with burns affecting >=40% of their total body surface area (TBSA). All of the patients underwent bronchoscopic examination, and eight patients with severe inhalation injury were excluded from this study. Four patients who were <12 years of age or had active withdrawal of care during the initial burn resuscitation were also excluded. Nine women and 27 men between the ages of 17 and 89 years with a mean age of 51.9 years were enrolled in the study. The burn extent ranged between 40% and 99% TBSA with a mean value of 65.2% and a mean full-burn thickness of 47.8%.

Patient Care

In our burn center, we mainly apply the HLS protocol to extensively burned patients who are directly transported. However, most of patients transported from other hospitals were already treated with Parkland’s formula, and we continued treatment using that formula. Consequently, 14 patients were entered into the HLS protocol group and 22 patients into LR solution group. No significant differences in gender, age, percentage of TBSA and percentage of full-burn thickness were observed between the two groups (Table 1). The HLS protocol is illustrated in Table 2. The treatment was initiated by HLS300, followed by HLS250, 200, and 150 for 48 hours after injury. Patients in the LR group were started with resuscitation fluid according to the Parkland formula using LR solution at 4 mL/kg per percentage of TBSA per 24 hours for thermal injury. The infusion rate was controlled to obtain urine volume with a goal of 0.5 to 1.0 mL/kg per hour. Colloid (albumin) was administered approximately 24 hours after admission. None of the patients received osmotic or loop diuretics for 24 hours after injury.

Estimation of IAP

All of the burn patients at risk for IAH and ACS were closely monitored for increased IAP until IAP was normalized or measurements were stable and the patients was no longer considered at risk for IAH. The IAP was estimated by measuring their intrabladder pressure in the manner described by Kron et al.12 and validated in a study by Iberti et al.13 Briefly, 50 mL of sterile saline was injected into the urinary bladder through an indwelling Foley catheter. The catheter was subsequently clamped immediately distal to the aspiration port, and a pressure transducer was connected to the aspiration port by an 18-gauge needle. The transducer was normalized to zero at the level of the pubic symphysis while the patient was maintained in the supine position, and the bladder pressure was then transduced. Only end-expiratory values were used in an effort to avoid interference from respiratory excursion of the diaphragm into the intraabdominal space. Multiple investigators have confirmed a high correlation of the bladder pressure determined by this method with the actual IAP.

IAH and ACS

We considered an IAP >30 cm H2O to be indicative of IAH. ACS was defined as IAH in association with a clinically tense abdomen in combination with high peak inspiratory pressures (PIPs) that compromised the ability to ventilate the patient or oliguria despite aggressive fluid resuscitation. In an attempt to decrease the elevated IAP, nasogastric decompression, sedation, and pharmacological paralysis were initially performed. Once the IAP exceeded 30 cm H2O, the IAH had progressed to ACS. Those patients who failed to rapidly improve after the institution of these conservative measures underwent abdominal escharotomies for abdominal decompression in the intensive care unit. Escharotomy with electrocautery under local or systemic anesthesia was performed on all of the patients.

Measurements and Calculations

Hematological and biochemical examination were performed. The time to develop ACS was recorded, and the urine output was also recorded hourly. The abdominal perfusion pressure (APP) was calculated as mean arterial pressure minus IAP. Pulmonary function was assessed by PIP, positive end-expiratory pressure, and the tidal volume, and the alveolar oxygen pressure or tension/fractional inspired oxygen ratio was calculated from blood–gas data. Pulmonary compliance was used to assess functional pulmonary mechanics and was calculated as the tidal volume divided by (PIP minus positive end-expiratory pressure).

Statistical Analysis

Statistical analysis was performed using Statview (SAS Institute Inc., Cary, NC). All of the results were expressed as the mean ± SD. The Student t test or the [chi]2 test was also used where appropriate, and p values <0.05 were considered to be significant.

RESULTS

Evaluation of Intravenous Fluid Volume and Urine Output

The amount of fluid infused and urine production during the first 24 hours are shown in Figure 1. The total infusion volume in the HLS group of 3.1 ± 0.9 mL/24 h per kg per percentage of TBSA was significantly lower than in the LR group at 5.2 ± 1.2 mL/24 h per kg per percentage of TBSA, whereas adequate urine production was maintained in both groups. By infusing HLS solution, the total amount of infusion volume per percentage of TBSA needed to obtain adequate circulatory function could be reduced by approximately 40%. Hematocrit as a parameter of circulating blood volume decreased with fluid resuscitation in both groups, but there was no significant difference 24 hours after injury (Fig. 2).

Sodium Load and Serum Sodium

In the present study, the HLS group showed a sodium load of 0.59 mEq/%TBSA per kg, which tended to be slightly lower than that in the LR group, 0.65 mEq/%TBSA per kg. However, there was no significant difference between two groups. In the LR group, the serum sodium concentration was between 136 mEq/L and 138 mEq/L 24 hours after injury in this study. On the contrary, in the HLS group, the serum sodium concentration increased to a peak of 150.7 ± 10 mEq/L 24 hours after injury, and then the gradient decreased to an acceptable value.

Occurrence of IAH

The individual percentage of TBSA and fluid volume for 24 hours are shown in Figure 3. In 11 of 14 patients (79%) of the HLS group, the amount of fluid could be reduced under the calculated Parkland formula indicated by the dotted line with adequate urinary output (Fig. 1). On the contrary, 20 of 22 patients (91%) in the LR group required more fluid than that indicated by the formula. Two of 14 patients (14%) in the HLS group and 11 of 22 patients (50%) in the LR group developed IAH within 20.8 ± 7.2 hours after injury. Of the patients with IAH, 10 required >350 mL/kg per 24 hours of fluid. Patients with a burn surface area of >85% and in whom volume sparing was unsuccessful despite HLS administration developed IAH. Eleven of the 13 patients who developed IAH died.

Abdominal Perfusion

The peak IAP 0 to 24 hours and 48 hours after injury is shown in Figure 4A. The LR group showed a significantly higher peak IAP during the first 24 hours than did the HLS group, reflecting the higher incidence of IAH mentioned above. The mean arterial pressure was approximately equal in both groups (data not shown). Therefore, APP was maintained at a higher level in the HLS group than in the LR group at 93.0 ± 21.2 versus 62.5 ± 19.4 mm Hg (Fig. 4B). Forty-eight hours after injury, the IAP in the LR group still tended to be higher, but this was no longer significant. The APP in the LR group, however, remained lower, and this was significant.

Pulmonary Function

All of the patients were maintained on intermittent mandatory ventilation with a 1:1 inspiratory-to-expiratory ratio. The peak PIP for 24 hours after injury was remarkably higher in the LR group than normal (Fig. 5A), showing values consistent with the development of IAH. Therefore, 24 hours after injury pulmonary compliance significantly decreased in the LR group more than in the HLS group (Fig. 5B). The alveolar oxygen pressure or tension/fractional inspired oxygen decreased additionally 24 and 72 hours after injury in the LR group, which required more fluid volume than did the HLS group (Fig. 5C).

DISCUSSION

In this study, we discovered beneficial effects of HLS treatment in extensively burned patients during their initial resuscitation period. The most important finding was that HLS resuscitation can reduce the risk of secondary ACS with lower fluid load in burn shock than can LR solution.

ACS is an important complication for critically ill patients who have undergone surgery.14 ACS without abdominal injury or surgery was described as secondary ACS by Maxwell et al.15 Patients with severe burns are also at risk for developing ACS because of the large volume of resuscitation fluid that is infused, abdominal wall compliance decrease, capillary leakage because of increased permeability, bowel edema, intraabdominal fluid, and other factors. For the patients with extended burns, ACS may occur during the resuscitation period,1,2,7,8,16 with endothelial leaking requiring massive infusion, or later during their hospital course because of sepsis.1,8 In this study, only extensively burned patients who could develop ACS during their resuscitation period were examined.

In 1994, Greenhalgh and Warden 1 first reported on five children who developed IAH with bladder pressures >30 mm Hg during the burn resuscitation period. For four of these five patients, the intrabladder pressure, arterial blood gas, and urinary output before and after decompressive laparotomy were described, in which hypercarbia and oliguria were improved with falling intrabladder pressure by abdominal decompression. In 1999, Ivy et al.3 documented the bladder pressure, PIP, tidal volume, and urine output before and after decompressive laparotomy in three adult patients with burns of >=70% TBSA who developed ACS during their initial resuscitation. In another study, Ivy et al.7 also reported that IAH occurred in 7 of 10 patients with burns covering >20% TBSA and that 2 of these patients developed ACS that required surgical decompression.

ACS requires immediate abdominal decompression.17 We also monitored the IAP as closely as possible, because IAH tends to quickly progress to ACS. Once IAH was observed, we attempted to perform nasogastric decompression, sedation, and pharmacological paralysis. If the above procedures were not effective, we considered prompt abdominal decompression to avoid multiple organ failure and death. On the other hand, it is possible that laparotomy may make wound management more difficult in severe burn patients. Therefore, Corcos and Sherman 2 attempted percutaneous drainage of peritoneal fluid as nonoperative decompression and noted a positive effect. Tsoutsos et al.6 described how escharotomy improved IAP in patients with full-thickness burns of the thoracic and abdominal area. Nonoperative decompression, however, did not always work effectively, because IAP elevation occurred secondary to bowel distension and bowel edema, as well as peritoneal fluid after severe burns.1,3 Later, Latenser et al.16 reported that percutaneous drainage was effective in four of nine patients with IAH but that laparotomy was required in the remaining five patients in whom IAH progressed to ACS in their pilot study.

The generalized increase in capillary permeability that occurs in severe burn patients can contribute to extensive edema formation and intraperitoneal accumulation of “third-space” fluid. Presumably, bowel edema and fluid translocation are additionally worsened by venous hypertension because of elevated IAP. We speculated that escharotomy or percutaneous drainage might prove to be effective in the reduction of IAP of burn patients if it breaks the vicious spiral mentioned above. If IAH occurs again after escharotomy or peritoneal drainage, open laparotomy, which is thought to be definitive therapy for ACS, is required to release the next factor, the fascia and peritoneum. Undoubtedly, abdominal decompression reduces the IAP and improves physiological parameters in burned patients with ACS.6–8,16 We also previously reported a detailed description of hemodynamic changes, including APP, cardiac output, pulmonary compliance, and oxygenation, in severe burn patients with ACS before and after abdominal decompression.5 However, a large extent of patients with ACS have a poor prognosis if it develops to ACS, especially for severely burned patients, because of the difficulty of wound maintenance and infection control though abdominal decompression improved physiologic parameters. In this study, the mortality rate of patients who developed IAH was very high, because only 2 of 13 patients survived. Therefore, we focused on the fluid-sparing effect of HLS treatment in burned patients and its potential protective effect from IAH. A large amount of fluid shifting to the third space is one of the most important factors responsible for IAH, and, therefore, the cumulative fluid load was examined to observe ACS in several studies. Friedrich et al.18 observed that burn patients tend to be administered fluid in excess of the Baxter formula, and they determined that large amounts of fluid contribute to abdominal and extreme compartment syndromes, as well as to pulmonary compliance. Corcos and Sherman 2 reported that three burned patients developed ACS after receiving 1.08 L/kg per 46-hour, 0.33 L/kg per 15-hour, and 0.47 L/kg per 29-hour infusion, whereas Hobson et al.8 reported that a mean of 237 mL/kg per 12-hour resuscitation fluid caused the development of ACS in their 10 patients. Ivy et al.7 pointed out that the maximal IAP was correlated with the infused fluid volume in their nine patients. We noted previously that extensively burned patients who required large volumes of fluid, especially that in excess of 300 mL/kg per 24 hours, show a high incidence of complication by ACS.19

In a recent study, a resuscitation regimen using 2,000 mL/24 hour of crystalloid and 75 mL/kg of fresh frozen plasma in combination was shown to decrease volumes of fluid in the resuscitation period for burned patients and result in a lower incidence of ACS.20 However, a large amount of fresh frozen plasma is required to maintain adequate circulation, and it may exacerbate of respiratory failure at the end of the edema phase of burn shock.

In the present study, it was confirmed that HLS treatment reduces approximately 40% of the initial 24 hours worth of resuscitation fluid to maintain the same level of urine output to LR solution treatment in the burn shock period. As a result, in the HLS group, oxygenation at 72 hours was significantly more favorable than in the LR group. Eighteen patients of 22 (82%) in the LR group required more fluid than that estimated by the Parkland formula, whereas 12 of 14 (86%) in the HLS group required less. Numerous investigators 11,21 reported that HLS treatment requires a minimum amount of fluid in the burn shock period because of the extracellular expander 9,20,22 and inotropic effects, among others.23,24 To date, the advantages of the fluid-sparing effect of HLS treatment on cardiovascular overload and pulmonary edema after burn shock or edema formation have mainly been discussed. We first focused on the effect of HLS treatment on the development of ACS in burned patients and analyzed its risk compared with that for LR solution therapy.

As shown in Figure 3, many patients who required >350 mL/kg per 24-hour fluid developed IAH regardless of whether they were treated by HLS or not. Especially in patients with >85% TBSA, HLS could not reduce the volume of resuscitation fluid below this level to avoid IAH. In this study, no IAH patients were observed under 60% TBSA in both groups. According to the above, we speculate that HLS treatment may prevent IAH/ACS only in patients with <85% TBSA and in whom HLS can reduce the resuscitation fluid to below the subthreshold (350 mL/kg per 24 hours) for development of IAH. Additionally, they are likely to develop IAH with less fluid as the percentage of TBSA increases. Abdominal wall compliance might be affected more as the extent of the burns increases. On the other hand, HLS treatment might not provide a good prognosis for all of the patients and should be carefully planned with frequent analysis of not only hourly urine output but also of serum electrolytes and osmolarity, water and electrolyte balance, and continual assessment of the patient’s clinical response to the treatment.10 In the present study, the serum sodium concentration was temporarily higher than normal values in the HLS group 24 hours after injury and subsequently returned to acceptable values. In particular, elderly patients sometimes suffer from dehydration or hyperosmolarity in their clinical course, and their HLS treatment needs to be interrupted. The HLS protocol might not be appropriate for elderly patients. In this study, patients in the LR group tended to be slightly older than those in the HLS group, which showed no significant difference.

In conclusion, HLS treatment allows extensively burned patients with lower fluid load in the burn shock period to be maintained and reduces the risk of low abdominal perfusion and secondary ACS under close monitoring.

ACKNOWLEDGMENTS

This work was supported, in part, by a grant from Marumo Research Foundation for Emergency Medicine.

REFERENCES

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3. Ivy ME, Possenti PP, Kepros J, et al. Abdominal compartment syndrome in patients with burns. J Burn Care Rehabil. 1999;20:351–353. Bibliographic Links [Context Link]

4. Wilson MD, Dziewulski P. Severe gastrointestinal haemorrhage and ischemic necrosis of the small bowel in a child with 70% full-thickness burns: a case report. Burns. 2001;27:763–766. [Context Link]

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DISCUSSION

Dr. Steven R. Shackford (Burlington, VT): Dr. Oda and his colleagues have shown, in a group of severely burned patients, that initial resuscitation with hypertonic solutions of varying sodium content and osmolarity reduces intraabdominal hypertension, improves abdominal perfusion pressure, improves pulmonary function, and reduces the incidence of abdominal compartment syndrome compared to resuscitation with Ringer’s lactate.

The father of the clinical use of hypertonic saline solutions for resuscitation was Bill Monafo, who advocated for their use in burn patients in the 1970s. I had the pleasure and the privilege to know Bill, and I am sure that he would appreciate this work, because one of Bill’s earliest observations was that patients receiving his solution of hypertonic saline required fewer escharotomies and were clinically less swollen.

The authors are to be commended for this work. I believe, however, that the work needs some clarification.

First, how were the patients allocated or assigned to each treatment group? Was there any randomization?

Second, in the abstract provided with the manuscript, the authors state that hemodynamic parameters and blood gas analyses were recorded. In the discussion, they state that in the hypertonic group, cardiovascular overload was milder. However, the authors provide no hemodynamic data or blood gas analysis to support their contention. Such data are necessary to justify these statements. Can you provide us with this data?

Third, Dr. Monafo sagaciously pointed out that solute-free water was the culprit in producing interstitial and intracellular swelling, and he repeatedly showed that the sodium load per percent burn in patients receiving hypertonic saline was equivalent to those receiving conventional resuscitation. How much sodium in milli-equivalents per percent burn was administered in each group, and was there any significant difference between the groups?

Fourth, hypertonic saline has been shown to expand the intravascular compartment by extracting water from cells down an osmolar gradient. You measured electrolytes and osmolarity but did not report the data. Such data are extremely important, not only to confirm the physiologic mechanisms involved, but also to determine the safety of the hypertonic solutions that you used.

Fifth, you have pointed out in the introduction that abdominal compartment syndrome can reduce abdominal perfusion pressure and lead to multisystem organ failure. Did any of the patients in your study develop multisystem organ failure? If so, was there a difference between the two groups?

Finally, what was the mortality rate in the two groups?

Dr. Jun Oda (Nagoya, Japan): It’s necessary to describe the assignments of the patients. In our burn center, we mainly apply the HLS protocol to extensively burned patients who are directly transported. But most patients transported from other hospitals are already started under the Parkland formula, and we continued treatment using lactated Ringer’s. Therefore, our assignment was random, but this is not a prospective study. I discussed the effect of HLS on cardiovascular overload in our paper. We recorded transitional central venous pressure, chest X-ray, and PaO2/FiO2 ratio as oxygenation.

P/F ratio was significantly higher 72 hours after injury, as shown in the slide. In this refilling period after burn shock, central venous pressure was higher in the lactated Ringer’s group. Some patients didn’t show sufficient urine output and demonstrated pulmonary edema with various degrees of severity, especially elderly patients.

Our data confirmed that overload volume was milder in the HLS group. But these are not new findings. Dr. Monafo and other investigators have pointed out that sodium load was equivalent in HLS protocol and conventional resuscitation. In the present study, the HLS group showed a sodium load of 0.59 mEq/%TBSA/body weight, which tended to be slightly lower than that in the lactated Ringer’s group, 0.65 mEq. There were also no significant differences between two groups. On the contrary, sodium load is 0.52 mEq/24h/%TBSA/body weight in the Parkland estimated formula.

The data on electrolytes are very important from the perspective of safety and applications of HLS protocol. In the lactated Ringer’s group, the serum sodium concentration was between 136 mEq/L and 138 mEq/L during the initial 72 hours after injury.

On the contrary, in the HLS group, the serum sodium concentration increased to a peak of 150.7 ± 10 mEq/L 24 hours after injury. Then the gradient decreased to acceptable value. On elderly patients, aged 68 with 51% dermal burn showed an extremely high sodium concentration over 170 mEq. In elderly patient, sodium output often impaired during the acute period of burn, which might be associated with capacity of renal function. Therefore, we consider that the HLS protocol should be applied to the elderly patient with particular care, since this protocol might not be adequate for these patients.

As Dr. Shackford commented, abdominal compartment syndrome can reduce abdominal perfusion pressure and lead to multisystem organ failure. After escharotomy or percutaneous drainage improved abdominal hypertension, if that occurs again, open laparototomy is thought to be required as the definitive therapy to release the fascia. In fact, in our patients, it was difficult to obtain informed consent to perform laparotomy for the patients whose prognosis was thought to be poor, and the laparotomy on burned skin makes wound maintenance very difficult. More than half of the patients with HLS obviously showed prolonged symptoms, such as hypoventilation, low cardiac output, and/or low urinary output, obviously. We found no difference between the two groups about multisystem organ failure with HLS. The mortality rate was very high as only two patients survived.

Therefore, we also considered prevention of ACS was an important factor in improving survival rate, especially in burned patients. In our data, HLS protocol was not adequately protective in extensively burned patients with more than 85% TBSA affected. However, for patients with less than 85% affected, HLS protocol is considered to have an advantage in deducing the risk of HLS.

Dr. Kevin J. Farrell (Atlanta, GA): I didn’t quite understand what you said about laparotomy. How many patients had to have their abdomen opened, and was there a difference in survival between the intraabdominal hypertension groups or different survival between the hypertonic saline groups, and did you have an upper limit of serum sodium that you cut it off and had to stop the hypertonic saline resuscitation?

Dr. Jun Oda (Nagoya, Japan): We have no patients who had laparotomies performed on them, because it was difficult to obtain informed consent to perform laparotomy as mentioned. In this study, the mortality rate of patient developed ACS was very high as only 2 of 13 patients survived. Therefore, we focused on the fluid-sparing effect of HLS treatment in burned patients and its protective effect from ACS. We do not have an upper limit of serum sodium as cut-off value to interrupt the HLS protocol, but we usually consider stopping the hypertonic saline resuscitation if affected sodium output is observed, added to progressive hypernatremia.

Dr. Jay A. Yelon (Valhalla, NY): Two quick questions, one is can you comment on how you titrated your IV fluids to maintain the urine output? It’s generally believed, or it’s at least my opinion, that the Parkland formula, if you follow it directly, will just give you too much volume and too much sodium, so that may be influencing some of your results.

The second thing is, I think no matter what IV fluid you use for resuscitation, there is some point in the resuscitation where serum oncotic pressure gets too low, and that’s the risk factor for getting you into trouble with intraabdominal hypertension, so I was wondering if you have any plans in the future or currently collect any data with regard to serum oncotic pressure in your patients that you are resuscitating.

Dr. Jun Oda (Nagoya, Japan): I agree that Parkland formula often lead over resuscitation if we follow it directly. As for the second question, because it is a retrospective study, not all patients observed oncotic serum pressure, actually. As for the first question, we changed fluid volume based on our observing urinary output hourly or every 30 minutes. As for the serum oncotic pressure, I think your comments are right and very important. Unfortunately, in this study, not all patients observed serum oncotic pressure.

Key Words: Secondary abdominal compartment syndrome; Burns; Hypertonic lactated saline; Resuscitation period; Abdominal perfusion

Hope this helps,

ACE844