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 a 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?
The patient was manifesting signs of elevated ICP. I am not sure any non invasive device (Invos) would have changed anything but the patient was clearly within the peak swelling window and considering her age and the limited amount of room to swell she would herniated very rapidly. A repeat CTH on 6/11 would have demonstrated this evolution prior to her full blown herniation.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Why was an diagnostic cerebral angiogram not performed.
What makes you a good expert for this case?
I am a neurointensivist and neuroendovascular surgeon and I treat AVMs routinely.
How often do you encounter cases similar to this one in your practice?
I see AVM patients in clinic atleast twice a month and I manage ruptured AVMs atleast once a month (I also manage ICHs on a daily basis).
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.
How often do you encounter cases similar to this one in your practice?
I take care of approximately 100 patients with ICH per year. I take care of approximately 100 patients with symptomatic intracranial hypertension per year.
Want to open a case or submit response?
Comments are accepted only from Neurology - includes all subspecialties experts.
Comments are accepted only from experts practicing in the following States: CT, NJ, NY.