Intraosseous ByAlfonso
Infusion of Fluids in the Initial Management Hypovolemic Shock in Young Subjects
L. Velasco,
Carlos Delgado-Paredes,
Josephine
and John M. Templeton,
Templeton,
of
Carmen K. Steigman,
Jr
Philadelphia, Pennsylvania l immediate aggressive fluid resuscitation of a child with life-threatening hemorrhagic shock provides the difference between life and death. Obtaining venous access in the hypovolemic child sometimes is difficult and time consuming. In order to evaluate the benefit of prehospital administration of intraosseous fluids into the tibia1 bone marrow as a method of gaining quick access to the systemic circulation and in resuscitating victims from severe hypovolemic shock, 13 puppies weighing 4.6 to 10 kg were subjected to progressive, controlled exsanguination until their mean arterial pressure (MAP) was 20% or less of their baseline MAP for 5 minutes (maxishock). Then an 16.gauge intraosseous needle was inserted into the tibia1 bone marrow and lactated Ringer’s solution was infused at 300 mm Hg of pressure until a volume three times the blood loss had been administered. The MAP, central venous pressure, arterial blood gases, hematocrit, serum lactate, and urine output were recorded at 10, 20, 30. 45. 60, 90, and 120 minutes after the onset of maxishock. At the end of the experiment the left lung of each animal was sent to the pathology department to investigate the possibility of bone marrow emboli. The results were compared with a group of control dogs with maxishock and no treatment, and a group of dogs with maxishock treated with a canine military antishock trousers inflated to 50 to 55 mm Hg and no fluids. The average needle insertion time was 16 seconds; the rate of infusion of fluids varied from a maximum of 25.7 mL/min to a minimum of 4.5 mL/min, with a mean of 10.6 mL/min. The overall survival, recovery of MAP, urine output, and lactic acid clearance were significantly better in the group of dogs treated with intraosseous fluids when compared with the other two groups. We conclude that the emergency administration of intraosseous fluids is both safe and efficacious in the initial resuscitation of hypovolemic shock when the intravenous route in the field is unavailable. Copyright o 1991 by W.B. Saunders Company INDEX WORDS: shock.
lntraosseous
fluid infusion;
hypovolemic
T
RAUMA, THE THIRD most common cause of death in all age groups, is the most frequent cause of mortality in children.’ In the prehospital setting, exsanguination is the second most common
From the Departments of Pediatric Surgery, Anesthesia, and Pathology, The Children’s Hospital of Philadelphia, and the University of Pennsylvania School of Medicine, Philadelphia, PA. Date accepted: March 20, 1990. Address reprint requests to John M. Templeton, Jr, MD, Department of Surgery, Children’s Hospital of Philadelphia, 34th & Civic Center Blvd, Philadelphia, PA 19104. Copyright o 1991 by EB. Saunders Company 0022-3468/91/2601-0002$03.00/0 4
cause of death.* The small and empty veins of children in hemorrhagic shock present a difficult problem to the paramedic team trying to obtain access to the circulation for administration of fluids and drugs. An alternative method in the field for emergency administration of fluids and medication when the preferred intravenous (IV) route fails, is the insertion of an intraosseous needle into the marrow of long bones. Long bones contain abundant marrow sinusoids that do not collapse during shock and drain into large medullary venous channels that, in turn, promptly empty into the systemic venous circulation via nutrient and emissary veins.3,4 Recently, several articles have appeared in the trauma literature reporting that the intraosseous method of administration of fluids has definite indications in the critically ill or injured pediatric patient in whom other, more conventional forms of access may not be available.’ A controversial issue with the intraosseous technique for administration of fluids is that flow rates obtained are not uniform and, in some instances, probably not fast enough to resuscitate victims from severe hemorrhagic shock.6 A preliminary study was designed to evaluate the efficacy of immediate administration of intraosseous fluids as a means of rapidly reversing severe hemorrhagic shock in order to improve blood pressure and prevent cardiac arrest and death in the critical 30 to 60 minutes following injury. This study was designed to simulate the prehospital setting in which IV access is not possible in a patient who is in profound shock and for whom the only modialities available to the paramedics are intraosseous access or military antishock trousers (MAST). We used a young canine model of controlled exsanguination to simulate profound hemorrhagic shock and then proceeded to resuscitate the dogs with the infusion of crystalloids through a needle inserted into the tibia1 bone marrow. We obtained hemodynamic and metabolic parameters at different time intervals and the results were compared with a similar group of dogs with controlled hemorrhagic shock that received no treatment, and a group of dogs with controlled hemorrhagic shock treated with MAST and no fluids. MATERIALS Thirty-nine were divided
AND METHODS
puppies, 6 to 12 weeks old, weighing 4.6 to 10 kg, into three groups. Puppies in all groups were
JournalofPediatric Surgery, Vol26, No 1 (January).
1991:
pp4-8
INTRAOSSEOUS
INFUSION
IN MANAGEMENT
OF SHOCK
anesthetized in the following manner: Innovar-Vet (Janssen, Piscataway, NJ), 0.1 mgkg, and Atropine, 40 l@kg, intramuscularly (IM); Pentobarbital 5 mg/kg, IV, over 10 minutes; Pancuronium, 1.0 mg, IV. Orotracheal intubation was done using a no. 5 cuffed endotracheal tube and ventilation was delivered at a tidal volume of 15 mL/kg at a rate of 20 per minute. Supplemental oxygen was given at 3.0 L/min. A peripheral IV line was inserted and normal saline solution was infused at 3.0 ml/kg/h. Under anesthesia the following catheters were inserted for hemodynamic monitoring: brachial artery line, internal jugular vein line with tip located in superior vena cava (SVC), femoral vein line with tip located in inferior vena cava (IVC), Foley bladder catheter, and rectal temperature probe. Following placement of all catheters, a second dose of Pentobarbital. 5 m&g IV, was given over 10 minutes. At baseline time and at defined time points after the onset of hemorrhage. the following hemodynamic and metabolic parameters were obtained: mean arterial pressure (MAP), SVC and IVC pressures, arterial blood gases, hematocrit. serum lactate, and urine output. After obtaining baseline parameters (time l), all puppies were subjected to controlled hemorrhage through the IVC catheter, initiated by withdrawing 5% (4 mL/kg) of the calculated total blood volume (TBV, 80 mL/kg) per minute, until 40% of the TBV had been withdrawn (time 2). Then a period of 5 minutes was allowed to compensate for the autotransfusion provided by contraction of the spleen (time 3). If at the end of the 5-minute waiting period the MAP was 20% of the baseline or below, we considered this to be a state of profound shock that we labeled maxishock (time 3A). However. if at the end of the 5minute waiting period the MAP was above 20% of the baseline, then every other minute, another 5% of the TBV was withdrawn. These 5% increments in TBV loss were stopped when the MAP finally reached a level of 20% or less of the baseline and could be sustained at this point for 5 minutes. With this method we achieved a standard insult due to hemorrhage in each dog. After the onset of maxishock, 13 dogs in the control group (group I) received no treatment and the aforementioned parameters were obtained at 10,20,30,45,60,90, and 120 minutes (times 4.5.6,7,8,9, and 10, respectively). In group II, immediately after the onset of maxishock, 13 dogs were treated with MAST and no fluids. The canine MAST was custom-designed by Jobst (Toledo, OH) for dogs weighing 4.5 to 10 kg, and was inflated to 50 to 55 mm Hg. Hemodynamic and metabolic parameters were obtained at the same time intervals as in the control group. Group III consisted of 13 dogs that after the onset of maxishock received treatment with lactated Ringer’s solution given intraosseously at 300 mm Hg pressure through a disposable 18-gauge intraosseous needle (Cook Group, Bloomington, IN) inserted into the tibia] bone marrow. A volume three times the blood loss was administered. The same parameters at the same time intervals as in the control group were obtained. At the end of the experiment, dogs in group III received a left pneumonectomy and the lungs were submitted for histological evaluation. The tissue sections were stained with hematoxylin and eosin and oil red 0 to show fat or bone marrow emboli. The results were analyzed statistically using Fisher’s exact test and t test.
100 90 80
70 60
%
Survival
50 40 30 20 10
OJ
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1
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5
6
7
8
9
10
Time intervals Fig 1. At 1 hour postmaxishock, MAST and intraosseous fluids improved survival (time 8). At 2 hours, only intraosseous fluids improved survival time (time 10). x, P = ,002; y, P = .0007; z, P = .0002.
during the administration of intraosseous fluids. The differential increment in MAP at times 4,5, 6, 7, and 8, was statistically significant between groups III and I (P < .005). The differential increment in MAP also had statistical significance between groups III and II at times 8, 9, and 10 (Fig 2). The urine output increased after the administration of intraosseous fluids, and this increment was statistically significant at times 5,6,7,8, and 9, when compared with groups I and II (P < .05). In group II, the urine output did not improve after the application of MAST despite the moderate improvement in MAP (Fig 3). Metabolic acidosis improved after resuscitation with intraosseous fluids. The increment in arterial pH was statistically significant at times 6 and 7 (P < .05) when compared with dogs in the control group. The difference in pH between groups I and II was not statistically significant (Fig 4). The decrement in serum lactate levels in
MAP
RESULTS
At 1 hour after the onset of maxishock, the mortality in group I (control) was 54%; in group II (MAST) 23%; and in group III (intraosseous fluids) 0%. At 2 hours after maxishock the mortality in group I was 85%: in group II 69%; and in group III it remained at 0% (Fig 1). The MAP was dramatically improved
04 1
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2
3
3A
4
5
6
7
8
9
I
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Time intervals Fig 2.
Effect of MAST and intraosseous fluids on MAP. lP < .005;
AP < .05.
6
VELASCO ET AL
25
20 h-l
cclmin
0.6
Serum
lactate
I-O
‘O-
MAST
I.‘-
,5 U.O.
a-
fluids
Controls
1
&
I I
/
I
1
2
3
3A
4
5
Time
Fig 3. Urine output traosssous fluids.
during
6
7
6
9
3
10
Time
intervals
resuscitation
with
MAST
and in-
group III was statistically significant when compared with groups I and II at time 8 (P < -05). The application of MAST in group II did not produce a decrement in serum lactate (Fig 5). The mean values for the hematocrit in group III were 29 at baseline, 23 during maxishock, and 17 after the administration of intraosseous fluids. Groups I and II showed a similar decrease in the hematocrit value from baseline to maxishock; however, the hematocrit did not decrease further after maxishock. In group III the insertion of an 18-gauge intraosseous needle into the tibia1 bone marrow was easy and fast. At autopsy, the tip of the needle was located in the center of the bone marrow in all 13 dogs and absence of extravasation of fluid was confirmed in all cases (Fig 6). The average needle insertion time was 16 seconds. The rate of infusion of fluids varied from a maximum of 25.7 mL/min to a minimum of 4.5 mL/min, with a mean of 10.6 mL/min. All dogs received a volume of crystalloids three times their blood loss in a minimum time of 28 minutes, a
6
3A intervals
Fig 5. Serum lactic acid levels during resuscitation rhagic shock.
from hemor-
maximum of 120 minutes, and a mean of 81 minutes after the onset of maxishock. Each dog in group III was well resuscitated according to the parameters evaluated. In the intraosseous group, sections of the left lung of each dog were taken from central and peripheral areas for histological study. In four dogs there were very small bone marrow emboli localized to medium and small peripheral vessels. The largest embolus measured approximately 700 x 200 pm. In one dog, a single, small bone fragment measuring approximately 150 x 100 km was found in a small peripheral vessel. DISCUSSION
The administration of fluids and drugs into the bone marrow of long bones is not a new procedure. It
7.45
pH
7.25 7.20
7.05
J
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:
:
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1
2
3
3A
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5
6
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6
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10
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Fig 4. Arterial pH during traosseous fluids versus MAST.
intervals
shock
and
resuscitation
with
in-
Fig 6. Postmortem view showing intramedullary of the intraosseous needle.
posftion of the tip
INTRAOSSEOUS
INFUSION
IN MANAGEMENT
OF SHOCK
was first described in 1927, by Drinker et al,’ and Doan,’ who independently demonstrated the use of this technique in animals. Papper in 1942, demonstrated that the circulation time of intraosseous and IV fluids was essentially the same,’ and Tocantis and O’Neill in 1941, popularized the clinical application of this technique.” The sporadic reports of osteomyelitis after long-term use of intraosseous needles” and the availability of better IV needles and catheters led to the abandonment of this technique. However, in the last 5 years the use of bone marrow for infusion of fluids and drugs in critically ill patients has experienced a resurgence, as noted in the emergency medicine literature.5.12 The intraosseous technique could prove of particular value in the treatment of the pediatric trauma victim at the scene of the accident and during transportation to a trauma center. The child with severe hemorrhagic shock often has flat and/or invisible peripheral veins that make the insertion of peripheral IV lines extremely difficult and time consuming. On the other hand, in human subjects the method of insertion of an intraosseous needle has been reported as simple and easily mastered.‘“,” Inserting an intraosseous needle into the tibia1 bone marrow secures a line away from the thorax where other resuscitative measures might be taking place. A critical factor with the intraosseous infusion of fluids is the rate of administration. Shoor et al, using a 13-gauge needle in a bovine model3 obtained flows of 10 and 40 mL/min under gravity and 300 mm Hg of pressure, respectively. Using an 1% gauge needle in small puppies, the present authors obtained a mean flow of 10.6 mL/min under 300 mm Hg of pressure. The flow rates varied from a minimum of 4.5 mL/min to a maximum of 25.7 mlimin. It is possible that the variable flows could be secondary to the final position of the tip of the needle within the bone marrow. Despite the variable flow rates, we were able to resuscitate dogs from profound hemorrhagic shock as evidenced by the improvement of MAP, increased urinary output, increased pH, and clearing of lactic acid. Also, a volume three times the blood loss was always delivered in less than 2 hours. The model used produced a uniform physiological insult due to profound hemorrhagic shock. However, it has the limitation of providing an arrested hemorrhage in which bleeding is stopped when a predetermined shock level is achieved. Despite this shortcoming, we think this model demonstrated the efficacy of intraosseous fluids in the early, rapid resuscitation of subjects in severe hypovolemic shock. The potential complications of the intraosseous
I
technique include osteomyelitis, subcutaneous abscess, extravasation of fluid into subcutaneous tissues, and fat embolism.‘3 However, the majority of complications have occurred in cases in which the intraosseous needle was left in place for prolonged periods of time. In the intraosseous group in this study, four cases of small bone marrow emboli and one case of a small bone fragment embolus in peripheral vessels of the lung were found. The clinical implications of this complication are not known. It is important to note the need for close monitoring when infusing intraosseous fluids under pressure. In one of the preliminary test dogs, the fluid bag emptied and an estimated 50 mL of air was infused into the marrow. The dog incurred an immediate cardiac arrest due to an acute air embolism. The main contraindications to the use of intraosseous fluids are fractured bones at the site of insertion, or the presence of localized cellulitis or infected burns. In order to prevent complications, the intraosseous route should be used only during acute critical situations and should be removed as soon as more conventional forms of venous access are available. The MAST suit, which has become a standard component of the prehospital armamentarium for the adult patient, has not been widely adopted in the pediatric population. It stabilizes fractures, promotes hemostasis, and elevates blood pressure mainly by increasing total peripheral resistance,ls thus improving circulation to vital organs during periods of shock. In this model, the use of MAST improved survival and MAP; however, it failed to improve urine output and acidosis. We conclude from this preliminary study that the infusion of intraosseous fluids is a fast and reliable technique for administration of crystalloid solutions. In a model of controlled, arrested hemorrhagic shock, the rates of infusion obtained were fast enough to achieve satisfactory resuscitation. The study was designed to simulate the prehospital setting of a patient with severe hemorrhagic shock for whom IV access is not possible. This study demonstrated that MAST alone is superior to no intervention at all, but that immediate intraosseous infusion of crystalloid is even more efficacious in regard to physiological resuscitation and prevention of arrest and death in the critical 30 to 60 minutes following injury. Subsequent studies will assess the efficacy of this approach in a model of active, continuous hemorrhagic shock. Finally, the data suggest the need for controlled, clinical trials to confirm the efficacy of immediate intraosseous fluid resuscitation in a prehospital setting.
VELASCO ET AL
REFERENCES 1. Accident facts. Chicago. IL, National Safety Council, 1982 2. Lewis FR: Pre-hospital trauma care, in Trunkey DD, Lewis FR (eds): Current Therapy of Trauma. Philadelphia, PA, Decker, 1984, pp l-6 3. Shoor PM, Berryhill RE, Benumoff JL: Intraosseous infusions: Pressure-flow relationships and pharmacokinetics. J Trauma 19~772-774,1919 4. Berg RA: Emergency infusion of catecholamines into bone marrow. Am J Dis Child 138:810-811,1984 5. Parrish GA, Turkewitz D, Skiendzielewski JJ: Intraosseous infusions in the emergency department. J Emerg Med 459-63, 1986 6. Hodge D, Delgado-Paredes C, Fleisher G: lntraosseous infusion flow rates in hypovolemic “pediatric” dogs. Ann Emerg Med 16:59-63, 1987 7. Drinker CK, Drinker KR, Lund CC: The circulation in the mammalian bone marrow. Am J Physiol62:1-8, 1922
8. Doan CA: The circulation of the bone marrow. Contrib Embryo1 14:27,1922 9. Papper EM: The bone marrow route for injecting fluids and drugs into the general circulation. Anesthesiology 3:307-312, 1942 10. Tocantis LM, O’Neill JF: Infusions of blood and other fluids into the general circulation via the bone marrow. Surg Gynecol Obstet 73:281-287,194l 11. Quilligan JJ. Turkel H: Bone marrow infusion and its complications. Am J Dis Child 71:457-465,1946 12. Rosseti VA, Thompson BM, Miller J, et al: Intraosseous infusion: An alternative route of pediatric intravascular access. Ann Emerg Med 14:885-888,1985 13. Hodge D: Intraosseous infusion: A review. Pediatr Emerg Care 1:215-218,1985 14. Inserson KV, Criss E: Intraosseous infusions: A usable technique. Am J Emerg Med 4:540-542, 1986 15. Kaback KR, Sanders AB, Meislin HW: M.A.S.T. Suit Update. JAMA 252:2598-2603,1984
Infusion of Fluids in the Initial Management Hypovolemic Shock in Young Subjects
L. Velasco,
Carlos Delgado-Paredes,
Josephine
and John M. Templeton,
Templeton,
of
Carmen K. Steigman,
Jr
Philadelphia, Pennsylvania l immediate aggressive fluid resuscitation of a child with life-threatening hemorrhagic shock provides the difference between life and death. Obtaining venous access in the hypovolemic child sometimes is difficult and time consuming. In order to evaluate the benefit of prehospital administration of intraosseous fluids into the tibia1 bone marrow as a method of gaining quick access to the systemic circulation and in resuscitating victims from severe hypovolemic shock, 13 puppies weighing 4.6 to 10 kg were subjected to progressive, controlled exsanguination until their mean arterial pressure (MAP) was 20% or less of their baseline MAP for 5 minutes (maxishock). Then an 16.gauge intraosseous needle was inserted into the tibia1 bone marrow and lactated Ringer’s solution was infused at 300 mm Hg of pressure until a volume three times the blood loss had been administered. The MAP, central venous pressure, arterial blood gases, hematocrit, serum lactate, and urine output were recorded at 10, 20, 30. 45. 60, 90, and 120 minutes after the onset of maxishock. At the end of the experiment the left lung of each animal was sent to the pathology department to investigate the possibility of bone marrow emboli. The results were compared with a group of control dogs with maxishock and no treatment, and a group of dogs with maxishock treated with a canine military antishock trousers inflated to 50 to 55 mm Hg and no fluids. The average needle insertion time was 16 seconds; the rate of infusion of fluids varied from a maximum of 25.7 mL/min to a minimum of 4.5 mL/min, with a mean of 10.6 mL/min. The overall survival, recovery of MAP, urine output, and lactic acid clearance were significantly better in the group of dogs treated with intraosseous fluids when compared with the other two groups. We conclude that the emergency administration of intraosseous fluids is both safe and efficacious in the initial resuscitation of hypovolemic shock when the intravenous route in the field is unavailable. Copyright o 1991 by W.B. Saunders Company INDEX WORDS: shock.
lntraosseous
fluid infusion;
hypovolemic
T
RAUMA, THE THIRD most common cause of death in all age groups, is the most frequent cause of mortality in children.’ In the prehospital setting, exsanguination is the second most common
From the Departments of Pediatric Surgery, Anesthesia, and Pathology, The Children’s Hospital of Philadelphia, and the University of Pennsylvania School of Medicine, Philadelphia, PA. Date accepted: March 20, 1990. Address reprint requests to John M. Templeton, Jr, MD, Department of Surgery, Children’s Hospital of Philadelphia, 34th & Civic Center Blvd, Philadelphia, PA 19104. Copyright o 1991 by EB. Saunders Company 0022-3468/91/2601-0002$03.00/0 4
cause of death.* The small and empty veins of children in hemorrhagic shock present a difficult problem to the paramedic team trying to obtain access to the circulation for administration of fluids and drugs. An alternative method in the field for emergency administration of fluids and medication when the preferred intravenous (IV) route fails, is the insertion of an intraosseous needle into the marrow of long bones. Long bones contain abundant marrow sinusoids that do not collapse during shock and drain into large medullary venous channels that, in turn, promptly empty into the systemic venous circulation via nutrient and emissary veins.3,4 Recently, several articles have appeared in the trauma literature reporting that the intraosseous method of administration of fluids has definite indications in the critically ill or injured pediatric patient in whom other, more conventional forms of access may not be available.’ A controversial issue with the intraosseous technique for administration of fluids is that flow rates obtained are not uniform and, in some instances, probably not fast enough to resuscitate victims from severe hemorrhagic shock.6 A preliminary study was designed to evaluate the efficacy of immediate administration of intraosseous fluids as a means of rapidly reversing severe hemorrhagic shock in order to improve blood pressure and prevent cardiac arrest and death in the critical 30 to 60 minutes following injury. This study was designed to simulate the prehospital setting in which IV access is not possible in a patient who is in profound shock and for whom the only modialities available to the paramedics are intraosseous access or military antishock trousers (MAST). We used a young canine model of controlled exsanguination to simulate profound hemorrhagic shock and then proceeded to resuscitate the dogs with the infusion of crystalloids through a needle inserted into the tibia1 bone marrow. We obtained hemodynamic and metabolic parameters at different time intervals and the results were compared with a similar group of dogs with controlled hemorrhagic shock that received no treatment, and a group of dogs with controlled hemorrhagic shock treated with MAST and no fluids. MATERIALS Thirty-nine were divided
AND METHODS
puppies, 6 to 12 weeks old, weighing 4.6 to 10 kg, into three groups. Puppies in all groups were
JournalofPediatric Surgery, Vol26, No 1 (January).
1991:
pp4-8
INTRAOSSEOUS
INFUSION
IN MANAGEMENT
OF SHOCK
anesthetized in the following manner: Innovar-Vet (Janssen, Piscataway, NJ), 0.1 mgkg, and Atropine, 40 l@kg, intramuscularly (IM); Pentobarbital 5 mg/kg, IV, over 10 minutes; Pancuronium, 1.0 mg, IV. Orotracheal intubation was done using a no. 5 cuffed endotracheal tube and ventilation was delivered at a tidal volume of 15 mL/kg at a rate of 20 per minute. Supplemental oxygen was given at 3.0 L/min. A peripheral IV line was inserted and normal saline solution was infused at 3.0 ml/kg/h. Under anesthesia the following catheters were inserted for hemodynamic monitoring: brachial artery line, internal jugular vein line with tip located in superior vena cava (SVC), femoral vein line with tip located in inferior vena cava (IVC), Foley bladder catheter, and rectal temperature probe. Following placement of all catheters, a second dose of Pentobarbital. 5 m&g IV, was given over 10 minutes. At baseline time and at defined time points after the onset of hemorrhage. the following hemodynamic and metabolic parameters were obtained: mean arterial pressure (MAP), SVC and IVC pressures, arterial blood gases, hematocrit. serum lactate, and urine output. After obtaining baseline parameters (time l), all puppies were subjected to controlled hemorrhage through the IVC catheter, initiated by withdrawing 5% (4 mL/kg) of the calculated total blood volume (TBV, 80 mL/kg) per minute, until 40% of the TBV had been withdrawn (time 2). Then a period of 5 minutes was allowed to compensate for the autotransfusion provided by contraction of the spleen (time 3). If at the end of the 5-minute waiting period the MAP was 20% of the baseline or below, we considered this to be a state of profound shock that we labeled maxishock (time 3A). However. if at the end of the 5minute waiting period the MAP was above 20% of the baseline, then every other minute, another 5% of the TBV was withdrawn. These 5% increments in TBV loss were stopped when the MAP finally reached a level of 20% or less of the baseline and could be sustained at this point for 5 minutes. With this method we achieved a standard insult due to hemorrhage in each dog. After the onset of maxishock, 13 dogs in the control group (group I) received no treatment and the aforementioned parameters were obtained at 10,20,30,45,60,90, and 120 minutes (times 4.5.6,7,8,9, and 10, respectively). In group II, immediately after the onset of maxishock, 13 dogs were treated with MAST and no fluids. The canine MAST was custom-designed by Jobst (Toledo, OH) for dogs weighing 4.5 to 10 kg, and was inflated to 50 to 55 mm Hg. Hemodynamic and metabolic parameters were obtained at the same time intervals as in the control group. Group III consisted of 13 dogs that after the onset of maxishock received treatment with lactated Ringer’s solution given intraosseously at 300 mm Hg pressure through a disposable 18-gauge intraosseous needle (Cook Group, Bloomington, IN) inserted into the tibia] bone marrow. A volume three times the blood loss was administered. The same parameters at the same time intervals as in the control group were obtained. At the end of the experiment, dogs in group III received a left pneumonectomy and the lungs were submitted for histological evaluation. The tissue sections were stained with hematoxylin and eosin and oil red 0 to show fat or bone marrow emboli. The results were analyzed statistically using Fisher’s exact test and t test.
100 90 80
70 60
%
Survival
50 40 30 20 10
OJ
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3A
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5
6
7
8
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10
Time intervals Fig 1. At 1 hour postmaxishock, MAST and intraosseous fluids improved survival (time 8). At 2 hours, only intraosseous fluids improved survival time (time 10). x, P = ,002; y, P = .0007; z, P = .0002.
during the administration of intraosseous fluids. The differential increment in MAP at times 4,5, 6, 7, and 8, was statistically significant between groups III and I (P < .005). The differential increment in MAP also had statistical significance between groups III and II at times 8, 9, and 10 (Fig 2). The urine output increased after the administration of intraosseous fluids, and this increment was statistically significant at times 5,6,7,8, and 9, when compared with groups I and II (P < .05). In group II, the urine output did not improve after the application of MAST despite the moderate improvement in MAP (Fig 3). Metabolic acidosis improved after resuscitation with intraosseous fluids. The increment in arterial pH was statistically significant at times 6 and 7 (P < .05) when compared with dogs in the control group. The difference in pH between groups I and II was not statistically significant (Fig 4). The decrement in serum lactate levels in
MAP
RESULTS
At 1 hour after the onset of maxishock, the mortality in group I (control) was 54%; in group II (MAST) 23%; and in group III (intraosseous fluids) 0%. At 2 hours after maxishock the mortality in group I was 85%: in group II 69%; and in group III it remained at 0% (Fig 1). The MAP was dramatically improved
04 1
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3
3A
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7
8
9
I
10
Time intervals Fig 2.
Effect of MAST and intraosseous fluids on MAP. lP < .005;
AP < .05.
6
VELASCO ET AL
25
20 h-l
cclmin
0.6
Serum
lactate
I-O
‘O-
MAST
I.‘-
,5 U.O.
a-
fluids
Controls
1
&
I I
/
I
1
2
3
3A
4
5
Time
Fig 3. Urine output traosssous fluids.
during
6
7
6
9
3
10
Time
intervals
resuscitation
with
MAST
and in-
group III was statistically significant when compared with groups I and II at time 8 (P < -05). The application of MAST in group II did not produce a decrement in serum lactate (Fig 5). The mean values for the hematocrit in group III were 29 at baseline, 23 during maxishock, and 17 after the administration of intraosseous fluids. Groups I and II showed a similar decrease in the hematocrit value from baseline to maxishock; however, the hematocrit did not decrease further after maxishock. In group III the insertion of an 18-gauge intraosseous needle into the tibia1 bone marrow was easy and fast. At autopsy, the tip of the needle was located in the center of the bone marrow in all 13 dogs and absence of extravasation of fluid was confirmed in all cases (Fig 6). The average needle insertion time was 16 seconds. The rate of infusion of fluids varied from a maximum of 25.7 mL/min to a minimum of 4.5 mL/min, with a mean of 10.6 mL/min. All dogs received a volume of crystalloids three times their blood loss in a minimum time of 28 minutes, a
6
3A intervals
Fig 5. Serum lactic acid levels during resuscitation rhagic shock.
from hemor-
maximum of 120 minutes, and a mean of 81 minutes after the onset of maxishock. Each dog in group III was well resuscitated according to the parameters evaluated. In the intraosseous group, sections of the left lung of each dog were taken from central and peripheral areas for histological study. In four dogs there were very small bone marrow emboli localized to medium and small peripheral vessels. The largest embolus measured approximately 700 x 200 pm. In one dog, a single, small bone fragment measuring approximately 150 x 100 km was found in a small peripheral vessel. DISCUSSION
The administration of fluids and drugs into the bone marrow of long bones is not a new procedure. It
7.45
pH
7.25 7.20
7.05
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:
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1
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10
Time
Fig 4. Arterial pH during traosseous fluids versus MAST.
intervals
shock
and
resuscitation
with
in-
Fig 6. Postmortem view showing intramedullary of the intraosseous needle.
posftion of the tip
INTRAOSSEOUS
INFUSION
IN MANAGEMENT
OF SHOCK
was first described in 1927, by Drinker et al,’ and Doan,’ who independently demonstrated the use of this technique in animals. Papper in 1942, demonstrated that the circulation time of intraosseous and IV fluids was essentially the same,’ and Tocantis and O’Neill in 1941, popularized the clinical application of this technique.” The sporadic reports of osteomyelitis after long-term use of intraosseous needles” and the availability of better IV needles and catheters led to the abandonment of this technique. However, in the last 5 years the use of bone marrow for infusion of fluids and drugs in critically ill patients has experienced a resurgence, as noted in the emergency medicine literature.5.12 The intraosseous technique could prove of particular value in the treatment of the pediatric trauma victim at the scene of the accident and during transportation to a trauma center. The child with severe hemorrhagic shock often has flat and/or invisible peripheral veins that make the insertion of peripheral IV lines extremely difficult and time consuming. On the other hand, in human subjects the method of insertion of an intraosseous needle has been reported as simple and easily mastered.‘“,” Inserting an intraosseous needle into the tibia1 bone marrow secures a line away from the thorax where other resuscitative measures might be taking place. A critical factor with the intraosseous infusion of fluids is the rate of administration. Shoor et al, using a 13-gauge needle in a bovine model3 obtained flows of 10 and 40 mL/min under gravity and 300 mm Hg of pressure, respectively. Using an 1% gauge needle in small puppies, the present authors obtained a mean flow of 10.6 mL/min under 300 mm Hg of pressure. The flow rates varied from a minimum of 4.5 mL/min to a maximum of 25.7 mlimin. It is possible that the variable flows could be secondary to the final position of the tip of the needle within the bone marrow. Despite the variable flow rates, we were able to resuscitate dogs from profound hemorrhagic shock as evidenced by the improvement of MAP, increased urinary output, increased pH, and clearing of lactic acid. Also, a volume three times the blood loss was always delivered in less than 2 hours. The model used produced a uniform physiological insult due to profound hemorrhagic shock. However, it has the limitation of providing an arrested hemorrhage in which bleeding is stopped when a predetermined shock level is achieved. Despite this shortcoming, we think this model demonstrated the efficacy of intraosseous fluids in the early, rapid resuscitation of subjects in severe hypovolemic shock. The potential complications of the intraosseous
I
technique include osteomyelitis, subcutaneous abscess, extravasation of fluid into subcutaneous tissues, and fat embolism.‘3 However, the majority of complications have occurred in cases in which the intraosseous needle was left in place for prolonged periods of time. In the intraosseous group in this study, four cases of small bone marrow emboli and one case of a small bone fragment embolus in peripheral vessels of the lung were found. The clinical implications of this complication are not known. It is important to note the need for close monitoring when infusing intraosseous fluids under pressure. In one of the preliminary test dogs, the fluid bag emptied and an estimated 50 mL of air was infused into the marrow. The dog incurred an immediate cardiac arrest due to an acute air embolism. The main contraindications to the use of intraosseous fluids are fractured bones at the site of insertion, or the presence of localized cellulitis or infected burns. In order to prevent complications, the intraosseous route should be used only during acute critical situations and should be removed as soon as more conventional forms of venous access are available. The MAST suit, which has become a standard component of the prehospital armamentarium for the adult patient, has not been widely adopted in the pediatric population. It stabilizes fractures, promotes hemostasis, and elevates blood pressure mainly by increasing total peripheral resistance,ls thus improving circulation to vital organs during periods of shock. In this model, the use of MAST improved survival and MAP; however, it failed to improve urine output and acidosis. We conclude from this preliminary study that the infusion of intraosseous fluids is a fast and reliable technique for administration of crystalloid solutions. In a model of controlled, arrested hemorrhagic shock, the rates of infusion obtained were fast enough to achieve satisfactory resuscitation. The study was designed to simulate the prehospital setting of a patient with severe hemorrhagic shock for whom IV access is not possible. This study demonstrated that MAST alone is superior to no intervention at all, but that immediate intraosseous infusion of crystalloid is even more efficacious in regard to physiological resuscitation and prevention of arrest and death in the critical 30 to 60 minutes following injury. Subsequent studies will assess the efficacy of this approach in a model of active, continuous hemorrhagic shock. Finally, the data suggest the need for controlled, clinical trials to confirm the efficacy of immediate intraosseous fluid resuscitation in a prehospital setting.
VELASCO ET AL
REFERENCES 1. Accident facts. Chicago. IL, National Safety Council, 1982 2. Lewis FR: Pre-hospital trauma care, in Trunkey DD, Lewis FR (eds): Current Therapy of Trauma. Philadelphia, PA, Decker, 1984, pp l-6 3. Shoor PM, Berryhill RE, Benumoff JL: Intraosseous infusions: Pressure-flow relationships and pharmacokinetics. J Trauma 19~772-774,1919 4. Berg RA: Emergency infusion of catecholamines into bone marrow. Am J Dis Child 138:810-811,1984 5. Parrish GA, Turkewitz D, Skiendzielewski JJ: Intraosseous infusions in the emergency department. J Emerg Med 459-63, 1986 6. Hodge D, Delgado-Paredes C, Fleisher G: lntraosseous infusion flow rates in hypovolemic “pediatric” dogs. Ann Emerg Med 16:59-63, 1987 7. Drinker CK, Drinker KR, Lund CC: The circulation in the mammalian bone marrow. Am J Physiol62:1-8, 1922
8. Doan CA: The circulation of the bone marrow. Contrib Embryo1 14:27,1922 9. Papper EM: The bone marrow route for injecting fluids and drugs into the general circulation. Anesthesiology 3:307-312, 1942 10. Tocantis LM, O’Neill JF: Infusions of blood and other fluids into the general circulation via the bone marrow. Surg Gynecol Obstet 73:281-287,194l 11. Quilligan JJ. Turkel H: Bone marrow infusion and its complications. Am J Dis Child 71:457-465,1946 12. Rosseti VA, Thompson BM, Miller J, et al: Intraosseous infusion: An alternative route of pediatric intravascular access. Ann Emerg Med 14:885-888,1985 13. Hodge D: Intraosseous infusion: A review. Pediatr Emerg Care 1:215-218,1985 14. Inserson KV, Criss E: Intraosseous infusions: A usable technique. Am J Emerg Med 4:540-542, 1986 15. Kaback KR, Sanders AB, Meislin HW: M.A.S.T. Suit Update. JAMA 252:2598-2603,1984
