So I am trying to wrap my head around the death of my patient and I thought maybe some of your opinions/ advice/ previous experiences could possibly help.
Pt was a female in her 40s, newly diagnosed in Nov. with HIV after being hospitalized for PCP pneumonia. She came into the hospital this weekend c/o headache, neck stiffness and general malaise. Was brought via EMS after syncopal episode while at the store. Mild SOB also noted. Pt placed on 4 li NC maintaining sats well, was sinus tach, BP normal, RR around 30 T max 99.5. A little lethargic but appropriate. Bloodwork sent and CT & MRI brain done which showed some diffuse cerebral edema. They were suspecting cryptococcal meningitis and atypical pneumonia and sent blood for cryptococcal antigen (later came back positive.)
So she ends up admitted to the tele floor but after a couple hours becomes increasingly short of breath and saturating about 84%. ABG normal except for low O2. She was placed on NRB and sent to me around 4 am. She did well on arrival and rested comfortably for a couple hours.
During the day she became increasingly tachypneic, was tried on BiPAP with no effect. Around 4 pm we electively intubated her to decrease her work of breathing. She was easily intubated after being given etomidate, versed and morphine I believe.
Approximately 20 min after intubation, she became bradycardic (40's). MD requested a 12 lead but in the 10 seconds it took to walk down the hall and get the machine she went into pulseless V tach. She was coded for 20 minutes- progressed from Vtach-> Vfib-> PEA-> Asystole.
Any ideas as to what happened? One person mentioned herniation as a possibility. Someone mentioned that a couple minutes into the code her pupils were fixed and unequal.
She ended up being a medical examiner case. When I called the ME, she decided to take the case because of the fact an LP was never done for the suspected meningitis.
Sorry I just wrote a small book :) Opinions/ comments much appreciated.
So I am trying to wrap my head around the death of my patient and I thought maybe some of your opinions/ advice/ previous experiences could possibly help.
Pt was a female in her 40s, newly diagnosed in Nov. with HIV after being hospitalized for PCP pneumonia. She came into the hospital this weekend c/o headache, neck stiffness and general malaise. Was brought via EMS after syncopal episode while at the store. Mild SOB also noted. Pt placed on 4 li NC maintaining sats well, was sinus tach, BP normal, RR around 30 T max 99.5. A little lethargic but appropriate. Bloodwork sent and CT & MRI brain done which showed some diffuse cerebral edema. They were suspecting cryptococcal meningitis and atypical pneumonia and sent blood for cryptococcal antigen (later came back positive.)
So she ends up admitted to the tele floor but after a couple hours becomes increasingly short of breath and saturating about 84%. ABG normal except for low O2. She was placed on NRB and sent to me around 4 am. She did well on arrival and rested comfortably for a couple hours.
During the day she became increasingly tachypneic, was tried on BiPAP with no effect. Around 4 pm we electively intubated her to decrease her work of breathing. She was easily intubated after being given etomidate, versed and morphine I believe.
Approximately 20 min after intubation, she became bradycardic (40's). MD requested a 12 lead but in the 10 seconds it took to walk down the hall and get the machine she went into pulseless V tach. She was coded for 20 minutes- progressed from Vtach-> Vfib-> PEA-> Asystole.
Any ideas as to what happened? One person mentioned herniation as a possibility. Someone mentioned that a couple minutes into the code her pupils were fixed and unequal.
She ended up being a medical examiner case. When I called the ME, she decided to take the case because of the fact an LP was never done for the suspected meningitis.
Sorry I just wrote a small book ? Opinions/ comments much appreciated.
Diffuse cerebral edema, bradycardia, unequal pupils.....recent c/o headache, neck stiff, and malaise....No LP done. A bit lethargic was past the time to intervene with the complaints suggesting meningitis- but should have been a big clue. LP should have been done. It will be interesting if the ME comes back with anything other than unilateral herniation. How sad.
There's no guarantee that even with aggressive intervention from the start that the outcome would have been good- I took care of a 20-something college student who ended up a quad/vent-dependent from meningitis that took her out at the C-1-2 level. TOTALLY alert and aware of what was going on- but couldn't move a thing besides her lips to "lip talk".... double major in college- wiped out.
But she might have had a chance. I wonder what the doc's reasoning was for NOT doing an LP..... If you find out what the post' results were, can you let us all know??? I'm sorry you ended up having to go through this as well. :hug:
Specializes in ACNP-BC, Adult Critical Care, Cardiology.
I think this patient is definitely sick and has a lot of reasons to become suddenly unstable to the point of arresting. Cryptococcal meningitis is a common opportunistic CNS infection with immunocompromised patients who have full-blown AIDS infection. It does present with AMS, symptoms of meningeal irritation (neck pain, photophobia), and diffuse cerebral edema on a Head CT. The diffuse cerebral edema could certainly lead to hydrocephalus and increased ICP and eventual brainstem herniation if the ICP becomes too high.
Etomidate was a good choice as an induction agent as it does decrease ICP and is ideal when intubating patients with neurologic problems and hemodynamic instability. But I also think your patient could be presenting with an ovewhelming sepsis likely from multiple sources (CNS and pulmonary being obvious ones) in the setting of being so immunocompromised. She was tachycardic, febrile, and though you didn't mention hypotension, she likely had other things that met SIRS criteria. Not knowing her cardiac function and volume status for sure, it could be possible that when she was intubated and sedated, her vasculature was relaxed to the point of worsening the vasodilatory effect of the ongoing sepsis, and she lost ability to compensate for the distributive shock with tachycardia so she ended up bradying down and going to into V-tach.
It's really all inferences on my part at this point but I think she certainly had all the reasons to be profoundly sick, code, and not have a good chance at survival given all the things that were done.
Wow, well I am sorry you are having to go through this. I reckon all involved are gonna have to wait it out for the ME report......
I don't understand how someone so stable can go south so quickly. How long was it from admit to code?
A cook at a place I used to work at never made it out of the ED with meningitis. They DID do an LP, but never got her stable enough to move- and she died after only a couple of hours in the ED (which is like no time w/all of the stuff going on). She'd been at work the day before. Cooking. In a nursing home.
Thank you all for the great responses! I really hope to find out what comes of the case, but this was my first patient death that wasn't cleared by the ME so I'm not sure if we get to hear of the results or not. The patient was actually a very close family member of someone who works on our unit so maybe they will mention something to us. Will definitely let you guys know!
I really appreciate all the great responses... Neuro is definitely not my strongest subject and I don't come across it much because our hospital has a Neuro/neurosurg ICU.
Juan de la cruz, I really appreciate the comment about the effects of the induction and RSI. I was wondering, since the code happened shortly thereafter, if the intubation may have had any effect in pushing her over the edge.
Meningitis is a terrible thing! Just last week a random person who saw me in scrubs out of work approached me about her daughter who was in an ICU with bacterial meningitis and what I thought her chances were. Sad.
I dont understand how someone so stable can go south so quickly. How long was it from admit to code?
You would be surprised! I've learned, in my short experience, not to trust any patient. I dont know how many times someone has said "this person is not that sick, why is he/she here (in the ICU)? And they never make it out of here.
And then I've seen people in MSOF, coded off and on throughout their ICU stay, walk out of the hospital.
The human body just compensates so well but can only do so for so long. When they decompensate, they tend to decompensate very quickly!
That does make sense....but bp, and rr at baseline? It is unusual to have high ICP with no signs of cushings triads?
Not trying to challenge here, trying to learn. We are being tested on this very topic tommorrow.
Cushing's triad is a LATE sign of increased ICP. Early signs are: headache, vomiting, lethargy/change in mental status, vision changes. I deal with increased ICP all the time working in neurology/neurosurgery and once patients present with signs of Cushing's triad we're running them to the OR ASAP.
Also, to the OP, was the patient started on antibiotics as soon as meningitis was suspected? We tend to put everyone with suspected meningitis on ceftriaxone and vanco until cultures are neg x 48 hrs.
I'm going to definitely agree with herniation in this case. I know the OP mentioned the baseline BP was 120/80, but any changes in the BP (narrowing PP)? What was the patients baseline LOC? OP mentioned lethargic but appropriate. Was the patient always lethargic? Change in LOC is the earliest sign of increased ICP...signs of Cushing's Triad (narrowed PP, bradycardia, irregular respirations) are a LATE sign of increased ICP. It's hard to determine irregular respirations if the patient is on the vent. Bradycardia? Definitely a part of the triad.
Anna Flaxis, BSN, RN
1 Article; 2,816 Posts
She had diffuse cerebral edema on CT. Cerebral edema=elevated ICP.