Inhalation injury treated with extracorporeal CO2 elimination

0 1997 Elsevier ELSEVIER

Burns Vol. 23, No. 4, pp. 354-359,1997 Science Ltd for ISBI. AU rights reserved Printed in Great Britain 0305-4179/97 $17.00 + 0.00

PII:SO305-4179(96)00111-8

Inhalation elimination E. Kornberger’,

injury

treated

I’. Mair’, E. Oswald’,

with extracorporeal

Ch. Hijrmannl

‘Department of Anaesthesia and Intensive Care Medicine, University of Innsbruck, A-6020 Innsbruck, Austria

A 38-year-old malewas admitted to the intensive care unit with a full-thickness burn involving 30 per cent of his total body surface area (TBSA) and severe inhalation injury. Respiratory failure developed within 54 h and CO, could not be eliminated, even by very invasive mechanical ventilation. Because of the patient‘s age and the minor extent of the burned TBSA, wc started extracorporeal CO, elimination (ECCOZ-R) and continued ECCO,-R for 30 days, when the patient was weaned from ECC. The clinical course during ECC02-R was complicated by major bleeding from a thoracotomy tube, from the site of tangential excision and by four septic episodes. Lung biopsy was performed twice on day 29 (during ECCO,-R) and day 58 (after ECCO,-R) after admission and revealed bronchiolitis obliterans without tendency to recozley. The patient died of sepsis with multiorgan failure on day 81 after trauma. 0 1997 Elsevier Science Ltd for ISBI. Key words: ECCO,-R)

inhalation

injuy, extracorporeal

Burns, Vol. 23, No. 4,354-359,

CO, elimination

1997

Introduction The combination of smoke injury and major burns is known to act synergistically in the pathology of lung injury’. Pulmonary complications are responsible for up to 70 per cent of deaths in burn injuries’. Therefore, management of the lung is crucial in treating patients with major burns. In recent years, extracorporeal methods to support gas exchange have been used more often in intensive care medicine. Until now the few case reports on extracorporeal circulation (ECC) methods in burn patients have shown a poor outcome (personal communications). Routine management, better technical equipment and heparin-coated cannulation sets have improved the performance of ECC, and ECC complications in intensive care patients have generally decreased.

Therefore, discussed inhalation

this therapeutic

method

again and implemented injuries. We describe

should

now be

in the treatment of our experience with

K. 6hlef

and ZDepartment

CO,

and D. Balogh’ of Reconstructive

Surgery,

ECCO,-R in a patient presenting with inhalation injury and a full-thickness burn cent of his total body surface area (TBSA), conventional therapy failed.

a severe to 30 per in whom

Case report A 38-year-old male was rescued from his burning car following an accident and admitted to the emergency department 6 h later. The patient had sustained full-thickness burns involving his head, face, both hands and the upper part of his back. TBSA was 30 per cent. The patient had been orotracheally intubated and ventilated at the scene of the accident. The patient’s haemodynamics were stable on admission [arterial pressure systolic/diastolic: 16/10 Wa (120/80 mmHg), heart rate: 1101. Initial blood gas analysis revealed a PaO, of 10.7 kPa (81 mmHg) at an FIO, of 0.6 and a PaCO, within the normal range. Upon admission, bronchoscopy showed a severe inhalation injury with necrosis of the mucosa involving the entire bronchial tree. The patient was ventilated in a biphasic positive airway pressure (BIPAP) mode, breathing on two different pressure levels, namely 3.4 and 2 Wa (25 and 15 mmHg) (Figure 1). As PaCO, increased continously up to 13.33 kPa (100 mmHg), we started ECCO,-R after 54 h to avoid further lung injury and barotrauma (Figure 3). We used two venous cannulas for venous access, advanced from both femoral veins to the upper and lower part of the V. cava. The blood circuit consisted of heparincoated silicone rubber tubing using a centrifugal pump. The patient’s blood was pumped through two parallel artificial lungs (Maxima Plus PRF Medtronic) and then returned to the patient (Figure 2). Low-dose heparinization was used to keep acute clotting time (ACT) at about 200 s; partial thromboplastin time (PTT) levels remained at the normal range (Table I). Various complications made ECCO,-R difficult: bleeding from a chest tube in the right pleural space, inserted because of effusion on day 7, necessitated two consecutive thoracotomies on days 10 and 16 after trauma to stop continuous blood loss. The chest tube caused emphysema

Komberget et al.: Inhalation injury treated with extracorporeal CO, elimination in the further course of treatment, necessitatingtwo more operations on days 29 and 68 of hospital stay. A transbronchial lung biopsy on day 29 after trauma again caused bleeding. Tangential excision of the burned surface was postponed until day 23 after admission.Despite ECCO,-R and low-dose systemichepa~nization, the burned skin had to be removed, becauseof major signs of wound sepsis. The operation was accompaniedby extensive blood loss(32 units of packed red cells and 10 units of fresh frozen plasma)(Figures 5 and 6). Lung function further deteriorated after the first surgical intervention and again during the septic episodes. ECCO,-R function was sufficient (Figure4): CO, elimination was excellent, and oxygenation within safe limits with PaO, values ranging between 9.33 and 20 kl’a (70-150mm %I.

355

After 30 days of ECCO,-R, the patient was weaned from the bypass.Although lung parenchyma had not recovered and compliancewas still low with values ranging between 25 and 31ml/cm HzO, CO, elimination was possiblewith mechanical ventilation alone (peak pressure: 30cm H,O, FIO,: 0.5-0.6, PEEP(positive end-expiratory pressure):5 cm H,O, ratio inspiration: expiration time: 1: 1 and 1: 2). Lung biopsy carried out on days 29 and 58 after admission revealed bronchiolitis obliterans without a tendency to recovery. Renal and cardiac failure developed and the patient died on day 81 after admission.

V-V - ECMO

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Baselinesetting Phigh = 30 I’ low= 10

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Figure 2. Schematicdrawing of ECCO,-R.

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COMPLlANCE

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TRAUMA

Figure 3. Patient’s PaO,, PaCO, and complianceduring the first 42 days following trauma.

HRS.

AFTER

TRAUMA

I 48

1

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356

Bums:

studiesduring therapy with ECCOz-l?.FIT = partial thromboplastin time

Table 1. Coagulation 1

---_.Days

after 3

2 3 4 5 6 7 8 9 10 11 12 73 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32

4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 36 27 28 XB

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trauma

1

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3: 89 90 84 77 75 84

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9

AFTER ECCOZ-R

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4

~

Fibrinogen

5 (%)

818 619 716 771 634 609 590 463 439 361 397 325 197 218 302 365 691 286 262 290 269 123 229 231 292 279 245 256 325 222 109 147

I 27

I 30

I 33

I 36

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100

94 90 54 83 43 71 81 73 80 62 60 93 108

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t

54h following trauma.

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CONTPLlANCE

9

(1 x 1000) 86 72 55 76 53 59 50 50 52 59 61 70 58 67 95 86 93 85 87 71 59 108 46 45 68 64 48 49 60 54 47 65

49 50 57 54 39 58 57 58 77 72 66 81 66 83 81 82 48 96

TRAUMA

Figure 4, Patient’s PaO, PaCO, and complianceduring the

6

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kPa

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DAYS

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95 88 i:

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Vol. 23, No. 4,1997

15

16

AFTER ECCO2-R

21

24

27

30

HZ0

33

TRAUMA 1

-J 36

357

Kornberger et al,: Inhalation injury hreated with extracorporeal CO, elimination

55 UNITS

OF PACKED

RED BLOOD

CELLS

50 HEMOGLOBIN

45

g I %

40 35 30 25 20 15 10 5 0 ,b

lb

DAYS r Figure 5. Blood loss and haemoglobin

0 Ellevels of the patient during

Discussion before ECCO,-R Our aim in ventilating the patient was to limit peak pressures to 30 cm water (to avoid barotrauma and pressure-induced injury to lung compliance) while applying high mean airway pressures. Therefore, we chose the BIPAP ventilation mode for artificial ventilation (Figure 2). BIPAP3 can be defined as pressurecontrolled ventilation with the advantage of unrestricted spontaneous breathing at any moment of the ventilation cycle. The duration of each phase as well as the corresponding pressure levels can be adjusted independently.

Ventilation

AFTER

I the first 40 days following

trauma.

With high PEEP levels, oxygenation could be maintained, but CO, removal became impossible with continuous detoriation of lung compliance. High PEEP levels depressed haemodynamics. The patient needed noradrenalin to stabilize at a MAP of 8 kl’a (60 mmHg). ECCOz-R As we agree with Rossair&, Gattinon? and Brunet6, who relate progressive lung injury to ventilatorinduced high pressures, we did not increase ventilatory peak pressure above 30 cm H,O. This resulted in a tidal volume of 300-500 ml, which yielded suffi-

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OF PACKED

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UNITS

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Figure 6. Number

6 5 101112131415161716192021

of platelets,

units of platelets

TRAUMA

and fresh frozen plasma during

extracorporeal

circulation.

1 X1 0000

CELLS PLASMA

358

Burns: Vol. 23, No. 4,1997

cient oxygenation, but caused PaCO, levels above 13.33 kPa (100 mmHg). The main entry criterion for extracorporeal respiratory support in our patient was therefore the impossibility of CO, elimination (Figure 3). Taking into consideration the patient’s FIO, of 1.0, his shunt fraction 30 per cent, his compliance ~20 ml/cm H,O, and the positive end-expiratory pressure 10 cm H,O, he met the commonly accepted entry criteria for extracorporeal membrane oxygenation 2.4,7,R. Results of application of ECCO,-R in our patient ECCO,-R supported ventilation and oxygenation for 30 days, keeping the blood gasesin the physiological range and gave the injured lung a chance to recover (Figure

4).

ECCO,-R allows a reduction in minute ventilation so that the injured lung can rest?. Even very invasive ventilation would never have managed CO2 elimination without high peak pressures and all concomitant complications like barotrauma and irreversible fibroplasia of the lung. We succeeded in keeping peak pressures at 30 cm H,O. Oxygenation was sufficient with an FIO, of 0.7; PaO, remained within safe limits, but varied between 9.33 and 22.7 kPa PaO,, (70 and 170 mmHg) due to septic episodes and bleeding after debridement of the burned surface area (Figure 4). Complications The severest complication seen in our patient was bleeding due to a chest tube and to debridement of the burned area. Patients on extracorporeal circulation are at risk of developing bleeding” due to a variety of factors, including heparinization and interaction with the surface of the Oxygenator’O. Platelets and clotting factors adhere to the prosthetic materiaP. After some days, saturation takes place and platelets then stabilize between 30000 and 60000, in our patient around 80000 (Figure 4 and Table I). Systemic low-dose heparin (1007 + 220 U/h) hardly influenced coagulation parameters (partial thromboplastin time = PTT 23-55 s Table 1). Before surgery, heparin was reduced to 500 U/h. Furthermore, we tried to optimize coagulation with platelets and fresh frozen plasma, therapy strategies also described by Firmin et al.“‘. The interaction between heparin-coated surface and various coagulation factors cannot be answered in detail. Pleural effusion compromised ventilation and oxygenation, and drainage appeared to be necessary. Bleeding from chest tubes is a dreaded complicatier?. As bleeding from the drainage site could not be stopped with conventional management’“, two thoracotomies had to be performed. The most extensive blood loss was due to excision of the burned body surface, which always requires a lot of blood substitutes even in a patient who is not on ECCO,-R. Stopping extracorporeal circulatory support during debridement was impossible at this time as the patient was dependent on ECCO,-R.

A further severe complication was infection with Staphlococcusaureus spreading from the drainage site. On ECCO,-R, infections are surprisingly rare2. Burn patients have impaired neutrophil functio+, T cells are decreased as well as immunoglobulinP. By days 6-7 after the trauma, bacteria are usually present in the burn wound and may induce a distant infection’. In addition, several reports describe a profound T cell lymphopenia in extracorporeal circulation’“. As complications like bleeding and infections jeopardized the success of ECCO,-R, we must examine whether these complications could have been prevented. Several episodes of major bleeding occurred, although heparin-coated sets with lowdose systemic heparinization were used for ECC and routinely performed coagulation parameters showed no major deterioration (Table I). Excision and covering of the burned surface should have been completed before initiating ECCO,-R. Drainage and all sorts of invasive tubes should be avoided in burn patients, because they are always prone to infections. In combination with ECCO,-R, this chest tube became the source of major unnecessary blood loss. Single puncture of the effusion could have relieved the lung and ensured oxygenation.

Conclusion ECCO,-R can be efficiently used for the treatment of inhalation injury to gain time for recovery, especially when it is associated with a minor burn trauma. Before initiating ECC, the full-thickness burned skin should be excised. Any drainage and invasive cannulation that is not absolutely necessary should be avoided. As the final outcome of the injured lung cannot be predicted, ECCO,-R therapy may be the last option in severe inhalation injury.

References 1 Strongin J, Hales AC. Pulmonary disorders in the burn patient. In: Martyn JA ed. Acute Management of the Burned Patient, 1st edn. Philadelphia, PA: Saunders Company, 1990; p. 25. 2 Cilley R, Bartlett R. Extracorporeal life support for respiratory failure. In: Gravlee GB, Davis RF eds. Cardiopulmonary Bypass, 1st edn. Baltimore: Williams and Wilkins, 1993, p. 665. 3 Hiirmann Ch, Baum M, Mutz NJ, Benzer H. Biphasic positive airway pressure (PIPAP) - a new mode of ventilatory support. Eur ] Anaestkesiol 1994; 11: 37-42. 4 Rossaint R, Lewandowski K, Papper D. Die Therapie des ARDS. 1. Teil: Aktuelle Behandlungsmethoden einschlieglich des extrakorporalen Gasaustausches. Anaestkesist 1994; 43: 298-308. 5 Gattinoni L, Pesenti A, Mascheroni D, Marcolin R. Low frequency positive-pressure ventilation with extracorporeal CO, removal in severe respiratory failure. JAMA 1986; 256: 881-886. 6 Brunet F, Belghith M, Mira J-P et al. Extracorporeal carbon dioxide removal and low frequency positive pressure ventilation. Chest 1993; 104: 889-897.

Kornberger et al.: Inhalation injury treated with extracorporeal CO, elimination 7 Snider MT, High KM, Campell DB. Extracorporeal membrane oxygenation. In: Hensley FA, Martin DE eds. A P7uc~jce of' Cardiac A~est~esja, 1st edn. Boston, MA Little Brown and Company, 1990; p. 662. 8 Zapol WM, Kolobow T. Extracorporeal membrane lung gas exchange. In: Crystal1 RG, West JB, et al. eds. The Lung, 1st edn. New York Raven Press, 1991; p. 2197. 9 Pesenti A, Kolobow T, Gattinoni L. Extracorporeal respiratory support in the adult. ASAIO Trans 1988; 34: 1~6-1008. 10 Firmin RK, Waggoner J, Pearson GA. Extracorporeal membrane oxygenation for neonates and older children, In: Lewis T, Graham TR eds. Mechanical Circu~#o~ Support, 1st edn. Boston, MA: Little Brown and Company, 1995; p. 78. 11 Fugate JH, Ryan Daniel P. Extracorporeal membrane oxygenation. problems in Anesthesia 1989; 3: 272-287.

359

12 Demling RH. Burns. In: Hall Jesse 8, Schmidt Gregory A, Wood DH eds. In: Principles of Critical Care. New York, St. Louis, San Francisco: MaeGraham Hill Inc., 1992; p. 817. 13 Pennington GD, Swartz MT. Infectious complications associated with ventricular assist device support. In: Lewis T, Graham TR eds. ~ec~ni~~ ~ircul~t~~ Sup~~o~t, 1st edn. Boston, MA, Little Brown and Company, 1995; p. 322.

Paper accepted 30 August 1996. Correspondence s~ozil~ be addressed to: Dr E. Kornberger, Klinik fur Anaesthesie and Allgemeine Intensivmedizin, Anichstrasse 35, A-6020 Innsbruck, Austria.