This is a memo relative to the case of a 20 yo young woman who was initially healthy, but developed intracranial bleeding found to be due to a small AVM. We would appreciate if you would please read the memo and let me know if this is a case in which there are departure(s) from the standards of care for which you would have both a Neuro ICU expert (for departures) and a neurology expert (for causation) available.
This is the case of a 20 yo healthy young woman who had a mild diffuse head ache for a day or two prior to 6/9/18. On the evening of Saturday, 6/9/18, she took a couple of Excedrin and napped on the sofa. While she was asleep, her mother observed seizure like movements and called the ambulance. She arrived at the Hospital 1 at 11:40 pm, and was found to be mildly postictal. A head CT revealed a 4.3 c 4.2 x 4.3 cm hemorrhagic mass versus hematoma in the left frontal region with surrounding edema causing mass effect upon the surrounding sulci and upon the anterior horn of the L lateral ventricle. There was a 7 mm shift of the midline structures from L to R, causing mass effect upon the anterior horn of the R lateral ventricle. The diagnosis was non-traumatic intracerebral hemorrhage. She was transferred by ambulance to Hospital 2 for further care, leaving Hospital 1 at about 3 am. She was completely awake and oriented and ambulatory by the time she left Hospital 1. VSS with BP 128/78, HR 82, RR 18.
She arrived at Hospital 2 on Sunday, 6/10/18 at 4:35 am, noted as alert & oriented x 3. She received 2 platelet infusions in the ER, one at 6:30 am, and the 2nd started at 8:55 am. A CT of the head done at 10:10 am revealed:
CT head findings: Non-contrast Head CT, CT angiogram & venogram head with contrast. Large acute hematoma anterior inferior L frontal lobe: approx. 42 x 39 x 38 mm, not significantly
changed from outside CT on 6/10/18 at 1:09 am. Mod amount of surrounding hypodensity, compatable with vasogenic edema. There is evidence to suggest delayed intracranial hemorrhage
Compared to prior study. There is severe mass effect with diffuse effacement of cerebral
sulci, partial effacement of L lateral ventricle, subfalcine herniation and L to R midline shift of approx. 8 mm, there is increased effacement of the L lateral ventricle compared to the earlier study.
A CT angiogram revealed: No evidence of intracranial aneurysm or high flow vascular
malformation; in the region of the large L frontal intraparenchymal hematoma no definite vascular malformation is ID’d. No CT angio evidence of active extravasation.
CT Venogram: Superior Saggital, straight transverse & sigmoid sinuses are patent, no evidence of dural venous sinus thrombosis.
The CT head impression was noted as “Large acute intraparenchymal hematoma L frontal lobe
The hematoma demonstrates heterogeneous signal characteristics which could represent mixed aged blood products or an underlying lesion.
The radiologist also noted that “hyperacute on acute hemorrhage can have this appearance, alternative diagnoses include: vascular lesion or underlying mass lesion. The radiologist also noted that “no evidence of large aneurysm or large AVM, however aneurysms <3mm may or may not be visualized utilizing CT angio technique”.
The recommendation was for MRI with and without contrast to exclude an underlying mass.
The patient was admitted to the neuro ICU on Sunday, 6/10/18 at 11:15 am. Her neuro exam appears to have been essentially normal, although she was noted as lethargic and drowsy, but Ox3, moving all extremities with good strength and no neuro deficits. At 12 pm, a Brain MRI with and without contrast was ordered as “urgent”. No MRI was done.
On Monday, 6/11/18, at 12:19 pm, the resident wrote an order for an MRI with and without contrast to r/o an underlying tumor, and for an angiogram on 6/12/18. No MRI was done on 6/11/18. At 4 pm, she was noted by the nurse as lethargic, arousable, VSS. At 8 pm, the nurse noted the patient was lethargic, slightly difficult to arouse, but Ox3 when awake. She noted sinus bradycardia on the CM monitor (HR 55-59) (was bradycardia caused by increasing intracranial pressure?) At 22:00 she noted the patient used the commode, complained of a HA at # 8 on 1-10 pain scale, was treated with 10mg oxy. The nurse also noted that the patient needed frequent reminding to leave the leads and pulse ox on. At 23:30, the nurse noted her as lethargic, sleeping for long periods, but Ox3 when awake, moving all extremities 5/5. At 00:00, she noted the pt’s headache was gone. At 2am, she noted ”neuro-assessment unchanged”, at 3:15 am, she noted the patient had once again removed her EKG leads, and had been incontinent of a large amount of urine, the patient stated she didn’t know why. Nurse noted her Ox3, following commands. 30 minutes later, at 3:45 am, she heard “banging noises” coming from the room, found the patient unresponsive, pupils at 5mm, nonreactive, and with snoring respirations.
At 4:00 the doctor was notified. The doctor noted patient likely having a seizure called for STAT intubation and CT scan. The CT scan done on 6/12/18 at 4:40 am revealed: Impression:
1) Continued evolutional changes of large left frontal lobe heterogeneous
Intraparenchymal hematoma, extending to the midline in the regions of the genu of the corpus callosum. Moderate amount
of surrounding hypodensity which is similar to mildly increased
in size and may represent vasogenic edema;
2) Interval increase in L to R midline shift increased L to R Subfalcine herniation; 3) New marked effacement of the suprasellar cistern compatible with herniation changes and likely new left uncal herniation. New effacement of the quadrigeminal plate cistern, as well as bilateral Cerebellar tonsillar herniation with crowding at the foramen magnum; 4) Persistent bilateral cerebral sulcal effacement which may Represent cerebral edema. Please correlate clinically for Increased intracranial pressures;
5) Interval enlargement of the R lateral ventricle compatible
With entrapment and evolving hydrocephalus.
After receipt of the CT scan results, Mannitol 20% IV solution premix 50 grams was ordered as a
Stat one time dose. At 5:30 am she was in the OR with anesthesia starting. A L craniotomy for
evacuation of intracerebral hematoma was performed. The surgical pathology noted the final dx
as “Hemorrhage, cerebral, Left (left sided hemcraniectomy); vascular malformation with
hemorrhage, recent, remote”.
Postoperatively, there was difficulty weaning from the vent. On 6/22/18, she was extubated, but
one hour later had to be re-intubated. She remained intubated until 7/3/18 when she was taken to
the OR for tracheostomy and PEG tube. During the postoperative period, from, June 13, 2018 through July 6, 2018, the daily ABGs except on 2 occasions document P02s of 116 to 154, mostly in the range of about 133, pHs for the most part at about 7.46 to 7.54, 02 sats 99.6 to 100.6. PC02s 18 – 35 on June 13 through June 19th, then 43 – 52 from June 20th through July 6.
She was discharged on 7/9/18 to inpatient rehab. She was discharged from rehab in September 2018, but continues to receive PT, ST and OT. She can walk, but relies on a wheel chair when outside the home. Her face is paralyzed, mostly on the left and she’s had significant loss of vision, and complete loss of color vision.
We have questions as to whether there were any departures in her care after she got to Hospital 2 that deprived her of the opportunity to avoid the severe change in her condition on the morning of 6/12/18 with what appears to be sudden worsening with herniation and her permanent
neurological injuries. For example,
1) Should this patient have been more closely monitored for increasing ICP with non-invasive Invos Cerebral Somatic Spectroscopy Monitoring device/machine, that was available at the time in the neuro ICU at Hospital 2?
2) Should hypertonic saline have been administered to keep further brain edema from developing, and thus to avoid increased ICP and/or to reduce ICP, particularly in view of the head imaging showing vasogenic edema and severe mass effect? (In this respect, please note that her serum sodium levels on 6/11/18 and 6/12/18 prior to her seizure at 3:45 am on 6/12, were noted as follows: 6/11/18, 10:31 am: 138; 6/11/18, 14:55: 132 (but the spec was noted as hemolyzed); 6/11/18, 18:40: 116 (again, the spec was noted as hemolyzed. A hemolyzed spec can cause an abnormally elevated K+, but can it also cause a lower than normal serum sodium value?); 6/11/18, 22:24: 136; 6/12/18, 2:28 am: 135; 6/12/18, 5:31 am: 131 (note, she was taken to the OR at about 4:30 am).
3) Was it a departure from the standard of care on Monday, 6/11/18 not to perform repeat head imaging such as CT scan or MRI to monitor for signs of increasing ICP, such as increased edema, mass effect?
4) Were the patient’s potential s/s of increasing ICP as reflected in the nurses notes on the
evening of 6/11/18 when she was noted with sinus bradycardia and more difficulty in
awakening her, indications for further studies at that time to assess for progression of the edema,
Bleeding, herniation? When she was incontinent of urine, was that a clue that she was getting
Worse? And if so, what if anything could have been done at that time, such as IV Mannitol, to change the outcome?
When she presented with these additional s/s was additional work up indicated for increasing ICP, and treatment with hypertonic saline and/or mannitol indicated prior to the seizure and massive brain herniation (after which she was treated with Mannitol?);
5) Should she have been taken to the OR sooner to remove the hematoma so as to avoid the herniation that eventually happened?
6) Post-operatively, in the days that followed, she was maintained in a hyperoxic state with blood gases showing persistent hyperoxia, was that within the standards of care? And can persistent hyperoxia cause and/or contribute to further worsening of a brain injury?
7) What departures do you see here, if any, that I did not comment on? And
8) is this a case in which you would feel comfortable being an expert?
Files:
No questions yet!
Do you believe there might have been medical error?
to answer your questions: 1. The patient was monitored in NeuroICU setting for ICP using a clinical exam. Doubt INVOS would have made a difference in the progression. 2. Depends on the degree of cerebral edema (present on admission). Pragmatically, HTS or mannitol only works in the setting of herniation when changes in Na occur rapidly at a rate of > 5mEq/L.. However, In this case, there is a degree of downtrend in Na from 138-> 131. This should have been avoided. 3. In my opinion a cerebral angiogram should have been performed earlier in this young individual. The etiology of ICH here is AVM. AVMs can be treated in some cases, specifically small aneurysms. Early eradication of AVM could have contributed to a better outcomes. However. There are risks involved in treating AVMs 4. YES 5. See #3. 6. Yes hyperoxia is associated with the worst outcomes after stroke (i.e. mortality). However, this signal has been seen in observational studies. Doubt it had any impact on this case, as she survided. Rincon F, Kang J, Maltenfort M, Vibbert M, Urtecho J, Athar MK, Jallo J, Pineda CC, Tzeng D, McBride W, Bell R. Association between hyperoxia and mortality after stroke: a multicenter cohort study. Crit Care Med. 2014 Feb;42(2):387-96. doi: 10.1097/CCM.0b013e3182a27732. PMID: 24164953. 7. Failure to diagnose AVM, potential to treat early. Failure to maintain eunatremia. Failure to recognize hydrocephalus. Failure to recognize high post-extubation failure. 8. I would need to review images, but my experience and expertise would fit. Final though need to review potential conflicts.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Failure to maintain eunatremia, would be associated with more cerebral edema. Failure to recognizes hydrocephalus to initiate external ventricular drainage. Since there was no re-bleed, the potential explanation for decompensation is hydrocephalus and metabolic disarray.
What makes you a good expert for this case?
Neurocritical care Neurology Vascular neurology
How often do you encounter cases similar to this one in your practice?
daily basis. we see a lot of ICH, AVM, SAH, stroke in the neuro ICU at my academic center.
Do you believe there might have been medical error?
1) Should this patient have been more closely monitored for increasing ICP with non-invasive Invos Cerebral Somatic Spectroscopy Monitoring device/machine, that was available at the time in the neuro ICU at Hospital 2? There is no evidence that such monitoring is associated with improved outcomes, and given that she had a good neurological examination to follow I do not think that any type of ICP monitoring was necessary in this case. 2) Should hypertonic saline have been administered to keep further brain edema from developing, and thus to avoid increased ICP and/or to reduce ICP, particularly in view of the head imaging showing vasogenic edema and severe mass effect? (In this respect, please note that her serum sodium levels on 6/11/18 and 6/12/18 prior to her seizure at 3:45 am on 6/12, were noted as follows: 6/11/18, 10:31 am: 138; 6/11/18, 14:55: 132 (but the spec was noted as hemolyzed); 6/11/18, 18:40: 116 (again, the spec was noted as hemolyzed. A hemolyzed spec can cause an abnormally elevated K+, but can it also cause a lower than normal serum sodium value?); 6/11/18, 22:24: 136; 6/12/18, 2:28 am: 135; 6/12/18, 5:31 am: 131 (note, she was taken to the OR at about 4:30 am). Although many clinicians would use hypertonic saline in this situation to maintain higher levels of sodium, there is not strong evidence for this practice. Therefore the absence of administration of hypertonic saline in this case would not be considered a violation of the standard of care. 3) Was it a departure from the standard of care on Monday, 6/11/18 not to perform repeat head imaging such as CT scan or MRI to monitor for signs of increasing ICP, such as increased edema, mass effect? Yes, I think this may have been a departure of standard of care, depending on the examinations as documented. She seemed to have an exam change by 4pm on 6/11/18 with more drowsiness, but it is not clear to me from the summary of events how severe this exam change was. If it was a clear deviation from her prior exam than a repeat CT scan would have been appropriate at that time. 4) Were the patient’s potential s/s of increasing ICP as reflected in the nurses notes on the evening of 6/11/18 when she was noted with sinus bradycardia and more difficulty in awakening her, indications for further studies at that time to assess for progression of the edema, Bleeding, herniation? When she was incontinent of urine, was that a clue that she was getting Worse? And if so, what if anything could have been done at that time, such as IV Mannitol, to change the outcome? When she presented with these additional s/s was additional work up indicated for increasing ICP, and treatment with hypertonic saline and/or mannitol indicated prior to the seizure and massive brain herniation (after which she was treated with Mannitol?); Sinus bradycardia is common in young patients, and I would need to know if this was new for her, as it may have been present without signifying any increase in ICP. The difficulty awakening her is more concerning. I think at that point she should have had a repeat CT scan, but again, the degree of mental status change is not entirely clear from the summary. There is no definitive data to support using hypertonic saline or mannitol in this initial time period, and I do not think that there was a deviation from standard of care by not administering these agents. 5) Should she have been taken to the OR sooner to remove the hematoma so as to avoid the herniation that eventually happened? It seems that once the worsening was discovered at 4:40am CT scan that she was in the OR within an hour, and had appropriately received mannitol at that point. Whether or not surgery should have been considered previously is more difficult to tell without seeing the imaging. 6) Post-operatively, in the days that followed, she was maintained in a hyperoxic state with blood gases showing persistent hyperoxia, was that within the standards of care? And can persistent hyperoxia cause and/or contribute to further worsening of a brain injury? This depends on the degree of hyperoxia. There is some data that it can worsen neurological outcomes, but it may be difficult to make a standard of care argument for this, especially given that recent trial data in post-cardiac arrest patients did not show a difference between the higher and lower oxygen groups that were tested. 7) What departures do you see here, if any, that I did not comment on? A young patient with no history of hypertension presented with a large cortical hemorrhage on 6/9/18. She already had a large amount of midline shift on the initial CT, raising the concern that she could develop uncal herniation, but she had an exam to follow. With 7 mm of rightward midline shift on arrival many practitioners would have thought that she might benefit from surgery initially, but most would be wary to do surgery without first having an angiogram due to the high risk of her having an underlying AVM. I am curious about the initial CTA, it's quality, and whether an AVM may have been missed. It is surprising that there was no angiogram able to be scheduled until 6/12, as the presence of a known AVM may have changed the view on early surgery for this patient. Additionally, it is not clear to me from the summary whether or not the CT head at 4:40am showed expansion of hematoma itself or just worsening edema.. If the hematoma did indeed expand, then not having done an angiogram previously is a problem as they could have potentially intervened on an underlying AVM to decrease the risk of recurrent bleeding. 8) is this a case in which you would feel comfortable being an expert? Yes, I would. However, I used to work in New York City, and so if this is for a hospital in New York City then it is possible that I could have a conflict of interest, depending on the institution.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
The patient clearly worsened neurologically and her ultimate exam and neurological deficits seem to be much worse than the exams leading up to the events of deterioration on 6/12 in the morning, and this correlated with worsened imaging findings.
What makes you a good expert for this case?
I am a board-certified neurologist and neurointensivist in active clinical practice, with experience working in both academic and non-academic centers. I have extensive experience in the evaluation of management of patients with intracerebral hemorrhage from various causes, including AVMs.
How often do you encounter cases similar to this one in your practice?
I see AVM-associated hemorrhages between 5-10 times per year in my practice.
Do you believe there might have been medical error?
I am a board certified neurologist and neurocritical care physician at an academic medical center. To begin with, there is equipoise when treating patients with intracerebral hemorrhage, especially those with underlying AVMs. 1. No. those are not standard of care and have uncertain reliability. 2. There is equipoise. Some physicians believe Na should be kept elevated, some believe it should only be elevated when patients develop signs and symptoms of symptomatic intracranial hypertension. 3. Imaging should be performed based on the patient's clinical symptoms, not purely to follow up prior imaging results. 4. Yes, she did have signs and symptoms of raised intracranial pressure, though this is in retrospect. It is uncertain whether hypertonics and mannitol would have significantly changed her outcome. 5. In retrospect, yes. 6. No. 7. Uncertain. 8. Yes, it is exactly the type of patient I take care of on a daily basis.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
1. No. those are not standard of care and have uncertain reliability. 2. There is equipoise. Some physicians believe Na should be kept elevated, some believe it should only be elevated when patients develop signs and symptoms of symptomatic intracranial hypertension. 3. Imaging should be performed based on the patient's clinical symptoms, not purely to follow up prior imaging results. 4. Yes, she did have signs and symptoms of raised intracranial pressure, though this is in retrospect. It is uncertain whether hypertonics and mannitol would have significantly changed her outcome. 5. In retrospect, yes. 6. No. 7. Uncertain. 8. Yes, it is exactly the type of patient I take care of on a daily basis.
What makes you a good expert for this case?
I am a board certified neurologist and neurocritical care physician at an academic medical center. To begin with, there is equipoise when treating patients with intracerebral hemorrhage, especially those with underlying AVMs. I have authored over 100 peer reviewed articles on brain injury. I have served as an expert on many cases and have provided live trial and deposition testimony for both the plaintiff and defense.
How often do you encounter cases similar to this one in your practice?
I take care of approximately 100 patients with intracerebral hemorrhage per year. I take care of approximately 100 patients with symptomatic intracranial hypertension per year.
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