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Altered mental status in an anticoagulated patient
The Journal of Emergency Medicine, Vol 15, No 1, pp 95-98, i9Y? Copyright 8 1997 Elsevier Science Inc Printed in the USA. All rights reserved 07x-4l>79/9?
ELSliiGER
s I7 00 -t .oo
PII SO736-4679(%)00262-4
C&se Resentations of TM Harvard EM Rw~cy ALTERED
MENTAL
STATUS
IN AN ANTKXIAGULATED
PATIENT
Eric S. Nadel, MD,’ David F. M. Brown, mt Department
of Emergency Medicine, ‘Brigham and Women’s Hospital and tMa.ssachusetts General Hospital. Harvard Medical School, Boston, Massachusetts Reprint Address: Eric S. Nadel, MD, Department of Emergency Medicine, Brigham and Women’s Hospital. 75 Francis Street, Boston, MA 02115
(Dr. Alasdair Conn) Was any history available pertaining to her hypercoagulable state? (Dr. Nadel) She was a patient of this hospital and had a history of hypercoagulable state of unknown etiology. Protein C, protein S, and antithrombin III levels were normal, and tests for the lupus anticoagulant and anticardiolipin antibody were negative. Her hypercoagulable state, therefore, was idiopathic. Intravascular coagulation had led to the bilateral above the knee amputations and an episode of mesenteric ischemia. She was maintained on a continuous heparin infusion at home to prevent further vascular thromboses. She had been treated with warfarin previously, which was discontinued after an episode of skin necrosis. Her past medical history also included a hysterectomy and bilateral oophorectomy, a retroperitoneal hematoma caused by angiography, and venous thromboses after central line placement. (Dr. John Gorry) Had any changes been noted in the days preceding the fall? (Dr. Nadel) There was no history of any behavioral change, fever, stiff neck, headache, or vascular problems prior to the fall. If there are no further questions, I will proceed with the case. Early in the course, there was concern as to how long the heparin infusion had been disconnected. Are there any thoughts on whether to restart the heparin? (Dr. Charles McCabe) I would be reluctant to restart the heparin without a better understanding of what
(Dr. Eric Nadel) Today’s case is that of a 50-yr-old woman who presented by ambulance after falling from her bed at home. She had been found awake and alert by her son, who called 911. She complained only of left hip pain and denied chest pain, shortness of breath, headache, nausea, vomiting, abdominal pain, or dizziness. She had a history of a hypercoagulable state and was maintained on a continuous heparin infusion at home. The EMTs noted that the intravenous heparin line had been disconnected, but the patient was unable to tell them for how long the line had been detached. Field transportation was uneventful, and on presentation to the emergency department (ED), the vital signs were: blood pressure, 112/80 mmHg; pulse, 96 beats/min; respirations, 16 breaths/min; and temperature, 37.1”C (98.9”F). Physical examination showed no signs of external head trauma. The tympanic membranes were normal. The patient’s neck was supple and without cervical spine tenderness. There was an old tracheostomy scar. The chest was not tender, breath sounds were clear and equal, and the abdomen was soft and nontender. The patient had bilateral above the knee amputations and severe tenderness of her left hip, with pain in the hip on motion. She was awake, communicative, and oriented x 3. She had word-finding difficulties, such as the inability to name common objects that were shown to her, but mental status was otherwise completely normal. Are there any questionsabout the initial presentation?
Case Presentations is coordinated by Eric S. Nadel, MD, of Brigham and Women’s Hospital, Harvard Medical School and by David F. M. Brown, MD, of Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts “-RECEIVED: 6 May 1996; ACCEPTED: 4 June 1996 95
96
kind of trauma she suffered. She was complaining of left hip pain and may have fractured her hip. In addition, despite the normal physical examination, she may have an intracranial hemorrhage because she must be assumed to have been anticoagulated at the time she fell. In such a patient, with a significant mechanism and even extremely subtle neurologic findings, a head computed tomography (CT) scan is indicated. (Dr. Nadel) We were concerned about the possibility of intracranial hemorrhage, although her neurological examination was nonfocal, and she was awake and oriented, with no headacheand no visible signs of head trauma. In fact, her only deficit was the word-finding difficulty. A CT scan was arranged immediately, and the patient went to the radiology suite. The heparin infusion was not restarted. While the patient was in CT, I learned from her private physician that she had had spontaneous arterial thromboses within 48 hours of cessation of anticoagulation but that venous thromboses had only occurred after procedures involving central venous access. After the CT scan, she proceeded to have plain radiographs of her left hip, which revealed an intertrochanteric fracture. While still in the radiology suite, she had a generalized seizure. (Dr. Richard Wolfe) You have to assume that this seizure is secondary to an intracranial hemorrhage. At the point she started seizing, you need to consider endotracheal intubation and how to control the seizures. (Dr. Nadel) Our approach at that point was to control the seizures and to obtain the results of the CT scan rapidly. We administered 4 mg of intravenous diazepam. (Dr. David Brown) The tracheostomy scar on her neck should alert you to the possibility of a difficult airway. Preparations should be made to perform a surgical airway if endotracheal intubation is unsuccessful. (Dr. Wolfe) I agree that airway control is indicated, but the question is, how best to do it? Both blind nasotracheal intubation and “awake” oral intubation are relatively contraindicated in patients with elevated intracranial pressure because of the tendency to raise the heart rate, blood pressure, and intracranial pressure. Ideally, one would like to use a controlled, rapid sequence technique, but the tracheostomy scar does indeed raise issues of a potentially difficult airway. (Dr. McCabe) One also would not want to nasally intubate a patient on heparin without knowing her partial thromboplastin time (PTT) . In fact, the PTT can be assumed to be elevated, making epistaxis much more likely to occur. (Dr. Wolfe) Coagulopathy is certainly one reason not to attempt nasotracheal intubation. I would argue that rapid sequenceintubation (RSI) is the method of
E. S. Nadel and D. F. M. Brown
choice, with the neck prepped to perform a surgical airway if oral intubation fails. (Dr. Nadel) During the seizure, she developed a supraventricular tachycardia ( SVT) at 180 beats/min, with a systolic blood pressure of 90 mmHg. The oxygen saturation was 90% on high flow oxygen. She was seizing and posturing. At this time, I was informed that the head CT scan revealed a subdural hematoma. (Dr. Wolfe) Did you treat the SVT or did you proceed with airway management at this point? (Dr. Nadel) We gave her 6 mg of intravenous adenosine, and she returned to a normal sinus rhythm at 80 beats/min, with a systolic blood pressure of 120 mmHg. Her seizure resolved after the diazepam was given. At this time, we proceededto managethe airway and I will ask Dr. Ron Walls to carry on from here. (Dr. Walls) The issues in this patient’s airway management have been articulated well. At this point, we have definite knowledge of an intracranial hemorrhage and can presume that intracranial pressure is elevated. The ideal method of intubation, as Dr. Wolfe stated, would be a controlled rapid sequencetechnique, augmented by lidocaine and a defasciculating dose of a competitive neuromuscular blocking agent. Fentanyl should be considered as a pretreatment agent to control the hemodynamic response to intubation. The issue of the potentially difficult airway is significant. One would not want to paralyze the patient and then be unable to intubate her. The big decision point for us rested on the ability to ventilate her. We felt that if intubation failed, but we were able to ventilate the patient by bag and mask, we would be able to proceed with a rescue strategy in an orderly fashion. We placed a bag and mask over the patient’s airway and tested our ability to ventilate her. She was easy to ventilate. This reassured us, and we proceeded with a rapid sequence intubation with a back up surgical airway. We premeditated with lidocaine 1 mg/kg intravenously (IV) to blunt the rise in intracranial pressure and gave fentanyl, 3 pg/kg, to blunt hemodynamic responses. Pancuronium 0.01 mg/kg IV was administered as a defasciculating agent, followed 3 minutes later by thiopental 3 mg/kg IV as an induction agent and succinylcholine 1.5 mg/kg IV to achieve paralysis. A number 8 endotracheal tube was passed without difficulty. Tube placement was confirmed with bilateral breath sounds, calorimetric end tidal CO2 determination, and chest radiograph. There were no further seizures. (Dr. Brown) You have another difficult decision to make regarding the status of her anticoagulation. Normally, in a heparinizedpatient with an intracranial hemorrhage, you would administer protamine. However, for this patient, rapid reversal of anticoagulation may cause
Altered Mental Status in Anticoagulated
Patient
thrombosis. Nonetheless,the intracranial hemorrhage is a greater immediate threat to her life than the possibility of arterial thrombosis, and I would favor giving her protamine. The usual dose of protamine is 50 mg given by slow IV injection over 10 min. More rapid administration can cause severe hypotensive and anaphylactoid reactions. Fifty milligrams of protamine will neutralize approximately 5,000 IU of heparin, forming an inactive heparin-pro&mine complex. In this case, because the patient has been off heparin for some time, 25 mg of protamine may be adequate. (Dr. Nadel ) Twenty-five milligrams of protamine were administered and neurosurgery was consulted. They elected for nonoperative management based on the fact that IV heparin would need to be resumed within the next 24-48 hours to prevent thrombosis. This would be contraindicated after a craniotomy. (Dr. Wolfe) Once the paralytic agents wore off, did a repeat examination suggest evidence of further neurologic deterioration? Was there a plan to place an intracranial pressure monitor and to obtain a repeat CT scan in a short period to see if midline shift was developing? ( Dr. Nadel) Her neurological deterioration did not progress. She was loaded with dilantin 15 mglkg IV. A repeat head CT scan was ordered. (Dr. McCabe) Did you obtain radiographs of the cervical spine’? (Dr. Nadel) When she arrived in the ED, she was awake, alert, oriented, and denied neck pain. She had no posterior neck tenderness or pain with range of motion of the cervical spine. We excluded cervical spine injury on clinical examination. Orthopedic surgery was consulted for the left hip fracture and conservative management was chosen. She had no further cardiac dysrhythmias and was admitted to the intensive care unit (KU). Follow-up CT scans revealed no expansion of the subdural hematoma. Heparin was restarted in the ICU. The patient’s mental status improved to baseline and remained stable while she was on the heparin infusion. She was weaned from the ventilator and discharged in stable condition to a rehabilitation hospital. ( Dr. Nadel) To summarize, this patient presented a number of clinical conflicts. First, I will ask Dr. Walls to discuss her airway management. Then, I will conclude with some comments on the priorities with regard to her hypercoagulable state. (Dr. Walls) Thank you. As was discussed previously, the patient had to be presumed to have a significant intracranial insult, with accompanying elevation of intracranial pressure (ICP). The optimum method of intubation in such circumstances is a modi-
97
fied rapid sequence technique incorporating pretreatment with lidocaine to attenuate ICP response to intubation, fentanyl to attenuate sympathetic response to laryngoscopy and intubation, and a defasciculating dose of a competitive neuromuscular blocking agent to attenuate the ICP response to succinylcholine. We would still argue that succinylcholine is the intubating neuromuscular blocking agent of choice for this and for virtually all emergency intubations because of its combination of cardiovascular stability. rapid onset, consistent effect, and short duration. The induction agent should be one that exerts its own cerebroprotective effect, and either etomidate or thiopental would be the best choice. The conflict in the airway is raised by the presence of the tracheostomy scar. At the time that the airway decision was being made, it was not known whether the tracheostomy had been elective or had been done as an emergency because of a failed intubation. Becausethe patient had had a tracheostomy rather than a cricothyrostomy, it was much less likely that the procedure had been performed in the emergency setting, where cricothyrostomy is a superior technique. Nevertheless, the risk of failure of intubation persists. The key issue in approaching the patient for RSI is whether one will be able to provide an airway and ventilate the patient in the event that intubation fails. A good approach in this circumstance is to test one’s ability to ventilate the patient using a bag and mask. When the mask was applied to this obtunded patient, it was easy for us both to assist her ventilation and to ventilate her independently between breaths. With this information in hand, we felt confident that in the unlikely event that intubation was uiisuccessful, we would be able to ventilate the patient adequately and to prevent the hypercarbia or hypoxemia that could exacerbate her head injury. (Dr. Nadel) The final issue is that of rhe anticoagulated state in the context of head injury. There are two important concepts here. The first is the presentation of the patient with a significant subdural hematoma with a modest mechanism of injury and virtually no symptoms. Anticoagulated patients are at high risk for intracranial hemorrhage after even moderate head trauma, and the CT scan was an essential part of her evaluation. If one was working in a hospital without CT scanning capability, consideration should be given to early protamine administration or fresh frozen plasma in the event of coumadin anticoagulation and transfer to a center with neurosurgical capability. This patient’s only neurologic abnormality was the wordfinding difficulty, but it was a definite and reproducible finding that must not be set aside. The second issue has to do with reversal of the anticoagulation. Admit-
98
tedly, this was a rather unusual case,with the idiopathic hypercoagulable state. However, the principles remain the same. The central issue is: what is the life threat? If the patient is more likely to die or suffer serious injury because of her anticoagulation than because of the condition for which the anticoagulation was pre-
E. S. Nadel and D. F. M. Brown
scribed, then reversal is indicated, with a plan to resume anticoagulation as soon as clinically reasonable. This was the opinion we held in this case, and so protamine was given. I would like to thank the participants, discussants, and audience for their insights.
ELSliiGER
s I7 00 -t .oo
PII SO736-4679(%)00262-4
C&se Resentations of TM Harvard EM Rw~cy ALTERED
MENTAL
STATUS
IN AN ANTKXIAGULATED
PATIENT
Eric S. Nadel, MD,’ David F. M. Brown, mt Department
of Emergency Medicine, ‘Brigham and Women’s Hospital and tMa.ssachusetts General Hospital. Harvard Medical School, Boston, Massachusetts Reprint Address: Eric S. Nadel, MD, Department of Emergency Medicine, Brigham and Women’s Hospital. 75 Francis Street, Boston, MA 02115
(Dr. Alasdair Conn) Was any history available pertaining to her hypercoagulable state? (Dr. Nadel) She was a patient of this hospital and had a history of hypercoagulable state of unknown etiology. Protein C, protein S, and antithrombin III levels were normal, and tests for the lupus anticoagulant and anticardiolipin antibody were negative. Her hypercoagulable state, therefore, was idiopathic. Intravascular coagulation had led to the bilateral above the knee amputations and an episode of mesenteric ischemia. She was maintained on a continuous heparin infusion at home to prevent further vascular thromboses. She had been treated with warfarin previously, which was discontinued after an episode of skin necrosis. Her past medical history also included a hysterectomy and bilateral oophorectomy, a retroperitoneal hematoma caused by angiography, and venous thromboses after central line placement. (Dr. John Gorry) Had any changes been noted in the days preceding the fall? (Dr. Nadel) There was no history of any behavioral change, fever, stiff neck, headache, or vascular problems prior to the fall. If there are no further questions, I will proceed with the case. Early in the course, there was concern as to how long the heparin infusion had been disconnected. Are there any thoughts on whether to restart the heparin? (Dr. Charles McCabe) I would be reluctant to restart the heparin without a better understanding of what
(Dr. Eric Nadel) Today’s case is that of a 50-yr-old woman who presented by ambulance after falling from her bed at home. She had been found awake and alert by her son, who called 911. She complained only of left hip pain and denied chest pain, shortness of breath, headache, nausea, vomiting, abdominal pain, or dizziness. She had a history of a hypercoagulable state and was maintained on a continuous heparin infusion at home. The EMTs noted that the intravenous heparin line had been disconnected, but the patient was unable to tell them for how long the line had been detached. Field transportation was uneventful, and on presentation to the emergency department (ED), the vital signs were: blood pressure, 112/80 mmHg; pulse, 96 beats/min; respirations, 16 breaths/min; and temperature, 37.1”C (98.9”F). Physical examination showed no signs of external head trauma. The tympanic membranes were normal. The patient’s neck was supple and without cervical spine tenderness. There was an old tracheostomy scar. The chest was not tender, breath sounds were clear and equal, and the abdomen was soft and nontender. The patient had bilateral above the knee amputations and severe tenderness of her left hip, with pain in the hip on motion. She was awake, communicative, and oriented x 3. She had word-finding difficulties, such as the inability to name common objects that were shown to her, but mental status was otherwise completely normal. Are there any questionsabout the initial presentation?
Case Presentations is coordinated by Eric S. Nadel, MD, of Brigham and Women’s Hospital, Harvard Medical School and by David F. M. Brown, MD, of Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts “-RECEIVED: 6 May 1996; ACCEPTED: 4 June 1996 95
96
kind of trauma she suffered. She was complaining of left hip pain and may have fractured her hip. In addition, despite the normal physical examination, she may have an intracranial hemorrhage because she must be assumed to have been anticoagulated at the time she fell. In such a patient, with a significant mechanism and even extremely subtle neurologic findings, a head computed tomography (CT) scan is indicated. (Dr. Nadel) We were concerned about the possibility of intracranial hemorrhage, although her neurological examination was nonfocal, and she was awake and oriented, with no headacheand no visible signs of head trauma. In fact, her only deficit was the word-finding difficulty. A CT scan was arranged immediately, and the patient went to the radiology suite. The heparin infusion was not restarted. While the patient was in CT, I learned from her private physician that she had had spontaneous arterial thromboses within 48 hours of cessation of anticoagulation but that venous thromboses had only occurred after procedures involving central venous access. After the CT scan, she proceeded to have plain radiographs of her left hip, which revealed an intertrochanteric fracture. While still in the radiology suite, she had a generalized seizure. (Dr. Richard Wolfe) You have to assume that this seizure is secondary to an intracranial hemorrhage. At the point she started seizing, you need to consider endotracheal intubation and how to control the seizures. (Dr. Nadel) Our approach at that point was to control the seizures and to obtain the results of the CT scan rapidly. We administered 4 mg of intravenous diazepam. (Dr. David Brown) The tracheostomy scar on her neck should alert you to the possibility of a difficult airway. Preparations should be made to perform a surgical airway if endotracheal intubation is unsuccessful. (Dr. Wolfe) I agree that airway control is indicated, but the question is, how best to do it? Both blind nasotracheal intubation and “awake” oral intubation are relatively contraindicated in patients with elevated intracranial pressure because of the tendency to raise the heart rate, blood pressure, and intracranial pressure. Ideally, one would like to use a controlled, rapid sequence technique, but the tracheostomy scar does indeed raise issues of a potentially difficult airway. (Dr. McCabe) One also would not want to nasally intubate a patient on heparin without knowing her partial thromboplastin time (PTT) . In fact, the PTT can be assumed to be elevated, making epistaxis much more likely to occur. (Dr. Wolfe) Coagulopathy is certainly one reason not to attempt nasotracheal intubation. I would argue that rapid sequenceintubation (RSI) is the method of
E. S. Nadel and D. F. M. Brown
choice, with the neck prepped to perform a surgical airway if oral intubation fails. (Dr. Nadel) During the seizure, she developed a supraventricular tachycardia ( SVT) at 180 beats/min, with a systolic blood pressure of 90 mmHg. The oxygen saturation was 90% on high flow oxygen. She was seizing and posturing. At this time, I was informed that the head CT scan revealed a subdural hematoma. (Dr. Wolfe) Did you treat the SVT or did you proceed with airway management at this point? (Dr. Nadel) We gave her 6 mg of intravenous adenosine, and she returned to a normal sinus rhythm at 80 beats/min, with a systolic blood pressure of 120 mmHg. Her seizure resolved after the diazepam was given. At this time, we proceededto managethe airway and I will ask Dr. Ron Walls to carry on from here. (Dr. Walls) The issues in this patient’s airway management have been articulated well. At this point, we have definite knowledge of an intracranial hemorrhage and can presume that intracranial pressure is elevated. The ideal method of intubation, as Dr. Wolfe stated, would be a controlled rapid sequencetechnique, augmented by lidocaine and a defasciculating dose of a competitive neuromuscular blocking agent. Fentanyl should be considered as a pretreatment agent to control the hemodynamic response to intubation. The issue of the potentially difficult airway is significant. One would not want to paralyze the patient and then be unable to intubate her. The big decision point for us rested on the ability to ventilate her. We felt that if intubation failed, but we were able to ventilate the patient by bag and mask, we would be able to proceed with a rescue strategy in an orderly fashion. We placed a bag and mask over the patient’s airway and tested our ability to ventilate her. She was easy to ventilate. This reassured us, and we proceeded with a rapid sequence intubation with a back up surgical airway. We premeditated with lidocaine 1 mg/kg intravenously (IV) to blunt the rise in intracranial pressure and gave fentanyl, 3 pg/kg, to blunt hemodynamic responses. Pancuronium 0.01 mg/kg IV was administered as a defasciculating agent, followed 3 minutes later by thiopental 3 mg/kg IV as an induction agent and succinylcholine 1.5 mg/kg IV to achieve paralysis. A number 8 endotracheal tube was passed without difficulty. Tube placement was confirmed with bilateral breath sounds, calorimetric end tidal CO2 determination, and chest radiograph. There were no further seizures. (Dr. Brown) You have another difficult decision to make regarding the status of her anticoagulation. Normally, in a heparinizedpatient with an intracranial hemorrhage, you would administer protamine. However, for this patient, rapid reversal of anticoagulation may cause
Altered Mental Status in Anticoagulated
Patient
thrombosis. Nonetheless,the intracranial hemorrhage is a greater immediate threat to her life than the possibility of arterial thrombosis, and I would favor giving her protamine. The usual dose of protamine is 50 mg given by slow IV injection over 10 min. More rapid administration can cause severe hypotensive and anaphylactoid reactions. Fifty milligrams of protamine will neutralize approximately 5,000 IU of heparin, forming an inactive heparin-pro&mine complex. In this case, because the patient has been off heparin for some time, 25 mg of protamine may be adequate. (Dr. Nadel ) Twenty-five milligrams of protamine were administered and neurosurgery was consulted. They elected for nonoperative management based on the fact that IV heparin would need to be resumed within the next 24-48 hours to prevent thrombosis. This would be contraindicated after a craniotomy. (Dr. Wolfe) Once the paralytic agents wore off, did a repeat examination suggest evidence of further neurologic deterioration? Was there a plan to place an intracranial pressure monitor and to obtain a repeat CT scan in a short period to see if midline shift was developing? ( Dr. Nadel) Her neurological deterioration did not progress. She was loaded with dilantin 15 mglkg IV. A repeat head CT scan was ordered. (Dr. McCabe) Did you obtain radiographs of the cervical spine’? (Dr. Nadel) When she arrived in the ED, she was awake, alert, oriented, and denied neck pain. She had no posterior neck tenderness or pain with range of motion of the cervical spine. We excluded cervical spine injury on clinical examination. Orthopedic surgery was consulted for the left hip fracture and conservative management was chosen. She had no further cardiac dysrhythmias and was admitted to the intensive care unit (KU). Follow-up CT scans revealed no expansion of the subdural hematoma. Heparin was restarted in the ICU. The patient’s mental status improved to baseline and remained stable while she was on the heparin infusion. She was weaned from the ventilator and discharged in stable condition to a rehabilitation hospital. ( Dr. Nadel) To summarize, this patient presented a number of clinical conflicts. First, I will ask Dr. Walls to discuss her airway management. Then, I will conclude with some comments on the priorities with regard to her hypercoagulable state. (Dr. Walls) Thank you. As was discussed previously, the patient had to be presumed to have a significant intracranial insult, with accompanying elevation of intracranial pressure (ICP). The optimum method of intubation in such circumstances is a modi-
97
fied rapid sequence technique incorporating pretreatment with lidocaine to attenuate ICP response to intubation, fentanyl to attenuate sympathetic response to laryngoscopy and intubation, and a defasciculating dose of a competitive neuromuscular blocking agent to attenuate the ICP response to succinylcholine. We would still argue that succinylcholine is the intubating neuromuscular blocking agent of choice for this and for virtually all emergency intubations because of its combination of cardiovascular stability. rapid onset, consistent effect, and short duration. The induction agent should be one that exerts its own cerebroprotective effect, and either etomidate or thiopental would be the best choice. The conflict in the airway is raised by the presence of the tracheostomy scar. At the time that the airway decision was being made, it was not known whether the tracheostomy had been elective or had been done as an emergency because of a failed intubation. Becausethe patient had had a tracheostomy rather than a cricothyrostomy, it was much less likely that the procedure had been performed in the emergency setting, where cricothyrostomy is a superior technique. Nevertheless, the risk of failure of intubation persists. The key issue in approaching the patient for RSI is whether one will be able to provide an airway and ventilate the patient in the event that intubation fails. A good approach in this circumstance is to test one’s ability to ventilate the patient using a bag and mask. When the mask was applied to this obtunded patient, it was easy for us both to assist her ventilation and to ventilate her independently between breaths. With this information in hand, we felt confident that in the unlikely event that intubation was uiisuccessful, we would be able to ventilate the patient adequately and to prevent the hypercarbia or hypoxemia that could exacerbate her head injury. (Dr. Nadel) The final issue is that of rhe anticoagulated state in the context of head injury. There are two important concepts here. The first is the presentation of the patient with a significant subdural hematoma with a modest mechanism of injury and virtually no symptoms. Anticoagulated patients are at high risk for intracranial hemorrhage after even moderate head trauma, and the CT scan was an essential part of her evaluation. If one was working in a hospital without CT scanning capability, consideration should be given to early protamine administration or fresh frozen plasma in the event of coumadin anticoagulation and transfer to a center with neurosurgical capability. This patient’s only neurologic abnormality was the wordfinding difficulty, but it was a definite and reproducible finding that must not be set aside. The second issue has to do with reversal of the anticoagulation. Admit-
98
tedly, this was a rather unusual case,with the idiopathic hypercoagulable state. However, the principles remain the same. The central issue is: what is the life threat? If the patient is more likely to die or suffer serious injury because of her anticoagulation than because of the condition for which the anticoagulation was pre-
E. S. Nadel and D. F. M. Brown
scribed, then reversal is indicated, with a plan to resume anticoagulation as soon as clinically reasonable. This was the opinion we held in this case, and so protamine was given. I would like to thank the participants, discussants, and audience for their insights.