A Case of Post-Traumatic Respiratory Failure

CLINICAL CONFERENCE IN PULMONARY DISEASE A Case of Post-Traumatic Respiratory Failure Clinical Conference in Pulmonary Disease from Northwestern University—McGaw Medical Center Chicago Co-Chairmen:

Douglas R. Gracey, M.D., F.C.C.P., Consultant in Pulmonary Medicine, Northwestern Memorial Hospital; Assistant Professor of Medicine, Northwestern University Medical School David A. Solomon, M.D., Trainee, U.S.P.H.S. Felhw in Pulmonary Medicine, Northwestern University Medical School David W. Cugell, M.D., F.C.C.P.; Chief, Pulmonary Section, Department of Medicine, and Ernest S. Bazley Professor of Medicine, Northivestern University Medical School

Dr. Gracey: The patient to be discussed today sustained multiple traumatic injuries and demonstrates the complex management problems of combined direct thoracic injury plus pulmonary complications secondary to extrathoracic injury. A 37-year-old truck driver drove into the rear of another truck at high speed. He was brought to the emergency room in a semiconscious state screaming, "help me, help me," but rapidly lapsed into coma. An endotracheal tube was inserted and the patient was put on a ventilator because of obvious multiple rib fractures and severe bilateral flail chest. The ventilator failed to overcome the flail chest, due in part to active spontaneous respirations. Pharmacologic suppression of the patient's breathing efforts was withheld pending neurosurgical consultation. Four towel clips were placed around the costal cartilages parasternally on the fifth and sixth ribs on both sides and traction was applied in an attempt to control the paradoxic motion of the chest. X-ray films revealed fractures of the right acetabulum, right femoral head, left femur, right tibia and fibula, several metatarsal bones, and at least five ribs plus the sternum. Many of the fractures were comminuted, and there was considerable displacement of many bone fragments. There were lacerations of the lower one-third of the right leg and right heel, Reprint requests: Dr. Cugell, Northwestern University cal School, 30.3 East Chicago Avenue, Chicago 60611

CHEST, 65: 3, MARCH, 1974

Medi-

with complete avulsion of the Achilles tendon. A small, left pneumothorax was suspected, and a needle placed in the left pleural space returned a minimal amount of air. It seemed likely that there were many more rib fractures than could be identified on the portable chest x-ray film. The appearance of the lung fields was compatible with contusion of both lungs (Fig 1 ) . Five units of whole blood were given in the 24 hours after admission. The systolic pressure never less than 60 mm Hg. On admission to intensive care unit the rectal temperature

first was the was

1. Chest roentgenogram taken at time of admission to hospital. Arrows indicate extensive subcutaneous emphysema and one of many anterior rib fractures. Irregular, bilateral infiltrates are beginning to appear. FICUFE

POST-TRAUMATIC RESPIRATORY FAILURE 323

38.88°C, the pulse rate 130/min and thready, and the blood pressure 64/40 mm Hg, The respiration rate exceeded 40/min, Subcutaneous emphysema was present bilaterally, and there was obvious paradoxic movement of the rib cage on both sides. A chest tube was inserted into the left side of the chest because of the minimal pneumothorax and because it was anticipated that prolonged mechanical ventilation with high inspired pressures would be required. A peritoneal tap was done to rule out intraabdominal bleeding and this was negative. The patient was taken to the operating room where his lacerations were debrided, closed loosely, and emergency treatment for his fractures carried out. A tracheostomy was performed over the endotracheal tube because prolonged need for an airway was anticipated.

normal. On the second hospital day the hemoglobin level was 10.1 gm percent, with a hematocrit value of 21 percent. By the next day the hemoglobin level was 8.3 gm percent. Let me digress a moment to discuss anticoagulation. On the first day the neurosurgeon attempted a spinal tap at the base of the skull because it was impossible to do a lumbar tap while the patient was in traction. The tap was traumatic. Therefore, anticoagulation therapy was not started on the first day. Heparin w as given on the second day, but this was discontinued two days later when the hemoglobin level dropped to 5 gm percent. The serum lipase value on the second hospital day was 3 units (the normal value is up to 1 unit). The initial electrocardiogram revealed an extreme right axis deviation, but three hours later the axis was normal.

The patient was returned to the intensive care unit and maintained on a volume ventilator at a respiratory rate of 20/min, with a tidal volume of 1,000 ml. His blood pressure remained normal after operation, and the pulse rate ranged from 125 to 130. Serum chemistry values were: calcium, 7.8 mg percent, (the lower limit of normal is 8 . 5 ) ; inorganic phosphate, blood urea nitrogen ( R U N ) , uric acid, cholesterol, total bilirubin, and alkaline phosphatase were normal; serum lactic dehydrogenase ( L D H ) , 320, (normal up to 2 2 5 ) ; and serum glutamic oxaloacetic transaminase ( S G O T ) 130, (normal up to 5 0 ) . W e attributed these enzyme elevations to his severe muscle trauma. The urine contained 1 + albumin, a large amount of occult blood, and 0 to 2 white blood cells per high power field. Six successive urine studies for stainable fat were negative. The admission hemoglobin and hematocrit levels were

Arterial blood gas values at 7:30 AM on the day of admission revealed: oxygen tension ( P 0 2 ) , 110 mm Hg; arterial carbon dioxide tension (Pcc-2), 50 mm Hg; pH, 7.14; and bicarbonate, 15.5 /xM/liter (Table 1 ) . At this point the patient was receiving 50 percent oxygen via a volume ventilator, but was not well controlled. He had a combined mild respiratory and rather severe metabolic acidosis. Two hundred and ninety mEq of bicarbonate were given over the next hour and by 2:00 PM, with no change in ventilator settings, there was a slight metabolic alkalosis (Table 1 ) . The P 0 2 was 291 mm Hg on 100 percent oxygen confirming a large degree of intrapulmonary veno-arterial shunting, (normal arterial P 0 2 while breathing 100 percent oxygen 550-600mm H g ) .

r

By 5.00 PM on the day of admission the metabolic alkalosis had increased slightly and the P 0 2 was

Table 1—Arterial Blood Gas Levels of Patient First Through Sixth Day of Hospitalization Admission

Second Hospital Day

7:30 AM

2 PM

110

291

81

63

68

58

50

39

39

41

41

7.14

7.50

7.59

7.52

Std. bicarb.*

15.5

29

35

Inspired 0 % * *

50

100

60

Time Po,, Hg Pco-2, mm P

Hg

H

2

5 PM

9 PM

9:40 AM

4 PM

8 PM

56

68f

103f

931

44

37

38

37

35

7.52

7.52

7.57

7.57

7.58

7.60

31

31

33

32

33

33

32

70

80

100

100

100

100

70

Third Hospital Day Time

9 AM

10 AM

Po , mm Hg

103f

111

P C O 2 , mm

34

pH

11 PM

8 PM

7 AM

9 AM

Fourth Day

Sixth

8 AM

2 PM

—

80

112

90

142

28

34

32

32

31

7.58

7.63

7.55

7.53

7.53

7.37

Std. bicarb.*

30

29

28.5

26

26

17.5

Inspired 0 % * *

60

60

50

50

35

30

2

Hg

2

*mM/liter; **Volume ventilator, 1,000 ml tidal volume; flO cm. HjO positive end-expiratory pressure (PEEP).

324

GRACEY, SOLOMON, CUGELL

CHEST, 65: 3, MARCH, 1974

adequate with 60 percent inspired oxygen. By 9:00 PM the P 0 2 was only 63 mm Hg on 70 percent 0 . Despite further increases in the inspired oxygen concentration, the arterial P 0 2 plummetted and the patient exhibited a rapidly progressive intrapulmonary shunt. By 7:00 AM the next day the P 0 2 on 100 percent oxygen was only 58 mm Hg (Table 1 ) . Positive end-expiratory pressure ( P E E P ) was instituted at 10 cm H 0 , while continuing the 1,000 ml tidal volume and 100 percent inspired oxygen concentration. A loading dose of 500 mg of hydrocortisone sodium succinate was given followed by intravenous administration of dexamethasone sodium phosphate 12 mg every four hours. By the end of the second hospital day the combination of PEEP, high inspired oxygen concentrations, and hydrocortisone resulted in a rapidly improving P 0 2 level. Hyperventilation was initiated in an attempt to keep the patient alkalotic so that he would not breathe spontaneously because of his flail chest. 2

2

On the morning of the third hospital day (Table 1 ) , the arterial blood values were such that P E E P was discontinued and by 2:00 PM the next day the inspired oxygen concentration was reduced to 35 percent. Three weeks after his injury the patient was weaned from the respirator. Throughout this period he was under complete ventilator control. The tracheostomy tube was removed one week later, and there were no signs of any residual paradoxic chest wall motion. The consulting neurosurgeon found no evidence of a subdural hematoma and attributed the coma to cerebral fat embolism. The patient regained full consciousness and was well oriented two and onehalf weeks after hospitalization. Three additional surgical procedures for definitive treatment of his multiple fractures were performed without complications and the corticosteroid therapy was gradually discontinued over a two-week period. In summary, this patient sustained multiple fractures resulting in probable pulmonary and cerebral fat embolism syndrome, and severe, bilateral flail chest. He was treated with controlled ventilation to overcome the flail chest, and with high inspired oxygen concentrations to counteract the effects of the severe veno-arterial shunting secondary to pulmonary fat embolism. Positive end-expiratory pressure was utilized during a period of severe hypoxemia to help maintain the arterial P 0 2 at an adequate level. High-dosage steroid therapy was used and probably contributed to the rapid improvement of his intrapulmonary shunt. After three weeks the ventilator was discontinued, and the tracheostomy tube was removed after four weeks. This patient had two life threatening major pulmonary problems: ( 1 ) biCHEST, 65: 3, MARCH, 1974

lateral flail chest and ( 2 ) intrapulmonary shunting secondary to probable pulmonary fat embolism. Dr. Solomon will discuss thoracic injury and additional details in the management of flail chest. Dr. Solomon: Thoracic injury can be divided into two broad categories: ( a ) penetrating and ( b ) crushing. Penetrating injuries are usually due to shrapnel, bullets, knife wounds, etc, and they maybe either closed or sucking. Crushing injuries, even if mild and with no loss of chest wall stability, may result in impaired respirations because of pain on breathing. With loss of rib cage rigidity, the respiratory complications are much more severe. Paradoxic chest wall motion may be expected whenever there are double fractures of three or more adjacent ribs. An anterior flail is the most common type seen following an automobile accident. The most frequent location is the lateral flail, usually seen in small children who are hit by an auto while running in the street. A posterior flail is least common. Although the mortality attributable to a flail chest per se is not known, 25 percent of all auto accident fatalities are probably due to crushing chest injury. - Fifty-five percent of people with crashing injuries of the chest have other major injuries and may die from shock, head trauma, pulmonary emboli, etc. Pulmonary edema and intrapulmonary bleeding also develop following severe crushing chest injuries. Whenever there is a paradoxic chest wall motion, the patient must generate an extremely high negative intrapleural pressure to inflate his lungs. The movable segment of the chest wall tends to collapse during inspiration and bulge out on expiration (eg, moves paradoxically). Much of the breathing effort is wasted moving deadspace air back and forth or from one lung to the other. 1

2

3

There are two cardinal principles in the treatment of flail chest: ( 1 ) establish an airway; and ( 2 ) positive pressure ventilation. A tracheostomy is best performed early, since prolonged ventilator therapy will be required, and removal of secretions is easier via a tracheostomy than through an endotracheal tube. If the area of paradoxic chest wall movement is small, endotracheal intubation and clearing of secretions may be sufficient, but with a large area of paradoxic chest motion a ventilator is always required. When it is not possible to maintain intubation and ventilation of the patient, the use of sandbags or otherwise applying pressure to the flail area may be tried. These stopgap measures have their limitations; the cough reflex is decreased, ventilation on the affected side is decreased, and there is no relief of the paradoxic motion during inspiration. Another form of therapy commonly used in the past was chest wall traction, and towel clips were placed around the ribs of this patient as an emergency measure. When left in place for weeks, the POST-TRAUMATIC RESPIRATORY FAILURE 325

clips cause infection or necrosis of the skin and they are very painful. The clips may cause a pneumothorax, hemothorax, and deformities if the traction is prolonged. Towel clip traction is now seldom used. Surgical fixation of the ribs may be helpful if there are lacerations of the lung or cardiovascular complications which require thoracotomy and the ribs are wired at the same time. Kirschner wires are useful in comminuted sternal fractures, but only if a ventilator is not available. Mechanical ventilation is the essential, lifesaving need in flail chest. Following the trauma, ventilation on the affected side is decreased because of splinting or paradoxic motion, secretions, pulmonary edema, bleeding into the lung parenchyma, and pneumothorax, all of which may be associated with the flail. With mechanical ventilation the fractured rib ends are better apposed than during spontaneous breathing efforts. The ventilator produces a positive pleural pressure, both on inspiration and expiration. Hyperventilation lowers the P C O 2 to a degree that inhibits spontaneous inspiratory efforts. This P C O 2 reduction and cessation of inspiratory effort is extremely important. It prevents inspiratory cave-in of the chest. The ribs move along their normal arc of motion, the rib end remains in apposition, and the fracture unites within two to five weeks. In most of our respirator patients, especially those with chronic obstructive lung disease, we avoid alkalosis because of the cardiac and central nervous system complications. Controlled hyperventilation is well tolerated by these patients and neither tetany, cardiac arrythmia nor convulsions develop despite the persistent alkalosis. Dr. Gracey: Apart from the lung damage secondary to direct thoracic trauma, there are numerous pulmonary complications of nonthoracic trauma including: traumatic wet lung, shock lung, and fat embolism. This patient also had bilateral pulmonary contusions. The development of a massive intrapulmonary shunt, the rapid response to therapy, the elevated serum lipase level, the reduced serum calcium level and his neurologic problem all suggested that he also had fat embolism of the lung. The pulmonary fat embolism syndrome is not well understood, but in my view occurs in the following manner: In the presence of a major fracture, neutral fat is released into the circulating blood (Fig 2 ) . Although it has been claimed that there is a de novo production of filterable fat in the blood due to the release of some factor from the broken bone, recent investigations have shown that the fat originates from bone marrow. Fat released into the venous circulation is filtered out in the pulmonary capillaries, but not all of the material is removed and some fat goes through to the systemic circulation (Fig 2 ) . Less than 25 percent of patients with pul4,5

326

GRACEY, SOLOMON, CUGELL

Phase

I;

Fracture

—Neutral

Fat

INF)

NF s e q u e s t e r e d

Phase

II:

MF

A \

IV

Phase

HF c o n v e r t e d

released

i n t o venous

i n pulmonary

to f r e e

fatty

capillary

acids

circulation bed

(FFA) by

lipase

Alcohol

III: Steroids i V — *

r — — \ /

Chemical

pneumonitis^—

Low Compliance,

incr.

Shunt

Platelet

thrombi

Low C o m p l i a n c e ,

incr.

Shunt

Lew Compliance,

incr.

Shunt

Heparin

/

I

FFAf

\ \

\

—

i, \

r

Reduced s u r f a c t a n t

Steroid* VOIUTO Venti l a t o r

_

-J, —

T

1

Stiff Lung Syndiome

. = Usudl \ \

Increased — — I n s p i red

°*

Hypoxemi a

sequence

= A l t e r e d sequence due t o t h e o r e t i c a l

LnVD = Low m o l e c u l a r w e i g h t

beneficial

drug

effect

dextran

FIGURE 2.

monary fat embolism have evidence of systemic fat embolization such as central nervous system manifestations, petechiae, stainable urinary fat, and fat globules in the retinal vessels. The eye grounds of our patient were difficult to examine because of facial swelling, but no fat globules were seen. No fat was found in our patient's urine, but his serum lipase level was elevated. The action of lipase produced by the lung on the neutral fat deposited in the pulmonary capillary releases free fatty acids ( F F A ) (Fig 2 ) , which permeate the alveolar-capillary membrane and alveolar space. If the F F A inactivates surfactant it would account for the typical time lag in the development of the intrapulmonary shunt in fat embolism syndrome. Surfactant lifespan is measured in hours and if surfactant production is cut off or altered, extensive microateleetasis develops. Free fatty acids are extremely irritating to the lung parenchyma and cause a severe chemical pneumonitis, platelet aggregation and microthrombi with microateleetasis. Many agents have been used to treat the fat embolism syndrome. One of the first drugs used was intravenously administered alcohol on the theory that it blocked lipase activity in the lung and thereby slowed the production of free fatty acids (Fig 2 ) . There is now considerable doubt as to the value of this method of treatment. Heparin was once thought to be useful because of its lipolytic action, but its major effect is now thought to be protection of platelets from aggregation and destruction. Both heparin and low molecular weight dextran have been used for this purpose. Steroids reduce the reactive chemical pneumonitis and these are the only drugs that have been shown both experimentally and clinically to be of value. 6,7

At present, steroids are undoubtedly useful in the CHEST, 65: 3, MARCH, 1974

treatment of this disease. Positive pressure ventilation with increased inspired oxygen concentration is essential if the clinical situation warrants. The other treatment modalities have not been proved to be of definite value, but they have not been disproved either. Dr. Solliday:* In view of the absence of retinal fat globules, urine fat, etc, what proof is there that this patient had the pulmonary fat embolism syndrome? This diagnosis is very hard to make and one is never sure which of the many causes of rapidly progressive intrapulmonary shunting associated with a "stiff lung" one is dealing with. Dr. Gracey: It is usually possible to sort out the pulmonary fat embolism syndrome from the many other causes for intrapulmonary shunting. There is a definite time lag between the trauma and the onset of a shunt. If you are successful, it rapidly reverses with therapy. I know this patient also had lung contusion, I did not feel that he had traumatic wet lung or shock lung. I doubt that either would respond to therapy as quickly and as well as did this patient. This man was never in a period of profound shock; his blood pressure was kept fairly normal except for a very brief period initially. You are correct in stating that the diagnosis of fat embolism syndrome is difficult to substantiate. Fortunately, we did not have the autopsy confirmation that we frequently have. Dr. Nam.-** It has been said that heparin therapy might have an adverse effect in that it may speed the conversion of neutral fats to free fatty acids, but I "Norman Solliday, M.D., Associate in Medicine, Northwestern University Medical School. " K e y I. Nam, M.D., Instructor in Medicine, Northwestern University Medical School; Assistant Director, Pulmonary Function Laboratory, Veterans Administration Research Hospital.

CHEST, 65: 3, MARCH, 1974

am not aware that this has ever been experimentally proven. Dr. Gracey: Our patient had both thoracic and extrathoracic reasons for the development of severe respiratory failure. W e have discussed the problems of flail chest and pulmonary fat embolism syndrome. Prolonged mechanical ventilation is essential for circumventing respiratory failure and chest wall stabilization. The diagnosis of pulmonary fat embolism is exceedingly difficult to make. Even if fat embolism is present, it is impossible to know if this is the major cause of the pulmonary physiologic deterioration in the individual patient or if other factors are operative. Fortunately, this patient survived both our therapy and ignorance. ACKNOWLEDGMENT: We gratefully acknowledge the technical assistance of Mr. Walter Hansen, Chief Therapist, Respiratory Therapy Department, Highland Park Hospital Foundation. REFERENCES

1 Avery E E , Head JR, Hudson TR, et al: The treatment of crushing injuries of the chest. Am I Surg 93:540, 1957 2 Hudson TR, McElvenny RT, Head JR: Chest wall stabilization by soft tissue traction. JAMA 156:768, 1954 3 Ashbaugh DG, Peters GN, Halgrimson CG, et a): Chest trauma. Arch Surg 93:540, 1967 4 Kerstell j , Hallgren B, Rudenstam CM, et al: The chemical composition of the fat emboli in the post-absorptive dog. Acta Med Scand (Suppl) 499:3-18, 1969 5 Hallgren B, Kersetell J, Rudenstam CM, et al: The influence of increased and decreased plasma free fatty acids on the formation and composition of the fat emboli in the dog. Acta Med Scand (Suppl) 499:43-56, 1969 6 Wertzberger JJ, Peltier L F : Fat embolism: The effect of corticosteroids on experimental fat embolism in the rat. Surgery 64:143, 1968 7 Ashbaugh DG, Petty T L : The use of corticosteroids in the treatment of respiratory failure associated with massive fat embolization. Surg Gynecol Obstet 123:493, 1966

POST-TRAUMATIC RESPIRATORY FAILURE 327