Clinical case 039: Ectopic ectopic – a Gedankenexperiment
This case starts with a bad gas. This patient arrived ‘in extremis’. Suspected ectopic transferred in by plane with the following data:
- Urinary HCG positive
- Abdominal pain for a few days
- No urine output for the last 24 hours
- Hb in the remote clinic was 130 g/l yesterday
- A 14 second US in ED showed a lot of free fluid, black with swirling clots in it….
She got an arterial line at the door and here is her opening ABG:
pCO2 = 58
pO2 = 255 (on rebreather 10L)
HCO3 = 10
BE = – 15
Na = 140
K = 8.9
Ca = 0.76
Glucose = 21 (~ 380 in the US)
Lactate = 10.5
Hb = 58 g/l (was 130 a few hours ago, and she has had 4 units PRBCs in transit)
The Obstetrician and Surgeon are there, keen to get in and control the bleeding ASAP. But I am a bit nervous about “whizzing her off to sleep” without a little more resus and think time.
So here are a few random questions about this case that I would like to hear your answers to.
- What drugs / agents would you want to give this patient before induction / intubation?
- What is you plan A for induction and intubation, including ventilator settings?
- What blood products / factors do you want to give in the next 30 minutes or so…?
Ok, those are the questions to ponder. Tough case. And that is all the info that was available at the time. Clearly not one where we can wait too long before jumping in and getting control. So what are you going to do?
Casey
First10EM Journal Club: January 2020
Clinical Case 048: We Ask an Epidural Expert
Countdown to SMACCUS
About The Author
Casey Parker
I am a GP working in Broome, NW of Western Australia. I work as a hospital DMO (District Med Officer) doing Emergency, Anaesthestics, some Obstetrics and a lot of miscellaneous primary care. Also on the web as @broomedocs | + Casey Parker | Contact
This is a terribly challenging case, the patient is basically peri-mortem.
Her gas tells a story; She’s hypovolemic (Hb 58), and as a result hypoperfused (BE -15 lactate 10.5). She has passed the tipping point, her capacity for compensation has been overwhelmed. Her CO2 of 58 is most worrisome, as her capacity for any sort of respiratory compensation has faltered and now, with mixed metabolic and respiratory failure she will rapidly die. Her pH of 6.9 and K of 8.9 and Ca of 0.76 are the immediate markers of that impending death.
She certainly requires resus prior to (or on the way to) theatre. My own (realistic) approach would be this;
1) IV access: She requires a large bore/cordis line in her IJ. This takes me about 60 seconds, and can be done as I am giving a first set of orders to my nursing team.
2) Metabolic derangements: The patient requires an immediate bolus dose of calcium chloride, and may well require repeat dosing. Insulin 10 units IV can be given for the hyperK, this will have minimal immediate effect but if the patient does survive to theatre it will be important. Bicarb probably has a role here in the setting of profound acidosis and profound hyperkalemia. I think there are some people who truly believe that bicarb is dead, but I would personally give it in this circumstance.
3) Volume resuscitation: I would treat this patient much like traumatic hemmorhagic shock with prolonged extraction time. The patient has severe anemia and we expect a consumptive coagulopathy. The patient has impaired ability to deliver oxygen to tissues as evidenced by her metabolic state. She requires some sort of balanced product resuscitation. Initially O-neg pRBCs are available and should be given by rapid transfusion. Plasma and platelets will also be required, the timeliness of their availability will vary tremendously based on where you practice.
4) Temperature management; Temperature management seems basic and we often don’t think much about it. I will suggest that this patients death is assured if active temperature management is not considered. This patient will become profoundly hypothermic as a result of her peri-mortem state, exacerbated by our exposure, and again by her laparotomy. She should be under a bair-hugger or similar warming device, and her fluids/ blood products should be administered via a warmer.
5) Induction for intubation and anesthesia. I don’t think there is a correct answer here, I would personally do either a fentanyl or etomidate as an induction agent. I would personally use fentanyl as it could be continued as an initial sole anesthetic agent (TIVA) in this case. I think paralysis with rocuronium is fine if you think you need it to get the airway here.
6) Vent settings; Luckily this patient seems like they probably have intact lungs (pO2 255 10l). I would initially match the vent settings to what I think someone with this patients metabolic status ought to look like. That is, some hyperventilation and probably slightly lower than average volumes. The FiO2 can and should be dialed back from 100%. In the long run if this patient survives there will be a period of ARDS requiring a protective strategy, but presently the patients lung function seems intact and can be used to support the remainder of her physiology.
7) This patient will probably die no matter what we do or how well we do it. It is important that the team caring for her is aware of this early in the case.
I am looking forward to hearing more!
Aaron
Blimey, you get all the good ones don’t you?
Well,I’ll answer on the fly so forgive me if not well-thought out.
Yes, she needs an eLap…but we could kill her with an anaesthetic so lets slow down a little and get some semblance of control.
Thoughts?
– she’s acidotic to buggery, anaemic and hyperkalaemic
So
-simultaneous assessment and treatment
– mobilise additional nursing staff, lab staff (transfusion) and let ICU know…we’re gonna need plenty of helpers…
Get on top of the K first – calcium gluconate 10mmol to stabilise myocardium, give insulin to drive K intracellularly (will help her hyperglycaemia) and also some bicarb. 12 lead ECG.
Large bore access if haven’t already. Swan sheath or rapid infuser catheter. Pop in a IJV central line (I’d go blind rather than faff with USS). Catheterise the bladder.
Blood bank notified, actuvate major transfusion protocol and start 1:1 packed cells/FFP. You’ve got baseline ABG inc calcium but add in coags and fibrinogen, repeatbhalf hourly. The lab tech is going to be flat out so will also need to have his/her second oncall available. Porters ready to convey ABGs and blood products to/from OT and the lab.
She’ll need RSI. You’d be brave to use sux in the context of hyperkalaemia so RSI with roc 1.2mg/kg and propofol, cricoid, secure airway then ventilate TV 5-7ml/kg aim ETCO2 ~35mmHg. Haven’t seen her BP but presume she’s hypotensive to acoid crash bolus propofol…don’t wanna be a propofol assassin. Can’t get my hands on thio currently. Could use ketamine, but don’t know her harmodynamics so have gone with the ajackson ajuice (cautiously)….that banging sound is Cliff Reid hitting his head aginst a wall, by the way.
Lines etc all easily available to me at head end, clearly marked and neat. Warm fluids through warmer, pop on a Bair hugger. If I’ve got a level one infuser and a nurse dedicated to run it, then use it.
Monitor temp, 30 minutely ABGs, monitor K/glucose/Hb/coags/calcium and Rx as appropriate…don’t want to get behind.
And change my underwear…
What a perfect JCCA Viva practice question! (Advanced level of course!!!)
First I would gently chuckle at the surgeon’s request to “whizz” her off to sleep. Nervous laughter always helps me.
I thought to this algorithm/approach when I was studying for my ViVA and it helps break it down for me.
Preoperative
Hx: Young lady, sick for few days, No U/O in last 24hrs
Ix: ABG as shown, Needs ECG!!!
Ex: Unsure… but likely in hypovolaemic shock (tachy + hypotensive ? likely level 4 loss)
Preop treatment: Calcium Gluconate 10% 10ml + Actrapid 10units then infusion 0.1units/kg
Diagnosis: haemorrhagic shock secondary to ruptured ectopic pregnancy (lost >40% TBV)
Anaesthetic Issues:
1) Anaemia: Hb 50something g/L and falling
2) Metabolic acidosis: hypoperfusion +hypoventilation
3) Acute renal injury – Pre-Renal – needs volume!!
3) Hyperkalaemia: likely due to acute renal injury, needs reversal
4) Hyperglycaemia:
Operative
Plan:
This lady needs to have haemostatic surgery preformed with concurrent resuscitation
Activate the massive transfusion protocol and get 4 PRC’s + 2 FFP’s up stat!
Call another anaesthetist/ friend to come and help you NOW!
Ketamine induction (1.5-2mg/kg) with Rocuronium 1.2mg/kg OR if unsure about special K, Fentanyl with titrated Propofol with a metaraminol chaser
Intubation Plan A: ETT Sz 7.5, Plan B Proseal with NGT maintaining cricoid until NGT is down, P
This is my sick person anaesthetic run through:
Airway: Positioned on bed for optimum laryngoscopy to GET THAT TUBE DOWN
Intubation plan as described above
Guedels in and tube secured
Breathing: Maintain oxygenation and normalize hypercarbia
Paralyse – keep nerve stimulator on to check through case
Volume control ventilation (7ml/kg TV) and hyperventilate to
ETCO2 ~ 35mmhg,
Fi02 (she is actually oxygenating well!) so… 0.4-0.5
ABG -> check another during the case to see where you are at
Circulation: Maintain BP and keep in sinus
Due to K+ have adrenaline drawn(1mg & 50mcg/ml) & defib in OT
Access!! At least 16G before anaesthesia and then another 14 or 16G
Fluids: Crystalloid 20ml/kg in ED and on way to OT then 15ml/kg,
Continue fluids
Consider CVL -> off to sleep first
Arterial line -> already in
Metaraminol infusion ready to go on induction and then titrate
Control Haemorrhage: Surgeons to their bit and I do mine (below)
Drugs +Glucose: Keep asleep, out of pain and normoglycaemia
Sevoflurane/Desflurane
Watch for signs of awareness -> HR/RR/Tears/Piloerection
Use BIS if you’d like
Insulin infusion (to lower K+ and BSL) -> check BSL q30min
Analgesia: Paracetamol + opioid (Fentanyl loading)
Environment: Keep warm and give antibiotics
Temp> 36c -> bair hugger and warmed fluids
Antibiotics as per surgical request + anaesthetic mx
Fluids/Renal: Give fluid, watch U/O, titrate and record
IDC placed
She is down at least 2L in blood volume and is dehydrated
Fluids 2L in ED/OT then another 2L in HDU over few hours
Check creatinine preop/post and K+ during case
K+: Insulin bolus then infusion, give HCO3 8.4%
Haem: Give blood and factors in goal directed sense
MTP activated: Transfuse 4 PRCS’s 2 FFP’s 1PLT -> delegate to your mate
Check bloods through case
Goals of resuscitation are: Temp >35, INR70g/L, Plt >50
Lactate<4.0, pH .7.2 and BE keep intubated and call ICU for help and RFDS for transfer likely during the case.
I’m going to add a bit more comment about my opinions about induction and RSI with this patient…
Here is Canada and the US I think almost everyone would use etomidate +/- roccuronium for RSI in a patient like this. I recognize that in much of the rest of the world etomidate is not available, and in some parts of the world anesthesia departments are still ‘not allowing’ the use of proper RSI drugs in the emerg.
If you don’t have etomidate in your dept. your RSI sequence for a patient like this requires a little more thought.
Ketamine is a consideration, but remember that it is not actually a hemodynamically neutral drug, rather it is a hemodynamically complex drug which causes an net neutral effect in terms of cardiac output. Ketamine is a direct myocardial depressant but also causes sympathetic nervous system activation resulting in an overall net neutral (or slightly positive) effect on cardiac output when used in a hemodynamically balanced patient (as for instance in ED sedation). With our patient above, I suspect that she is already maximally sympathetically driven or she has relative catecholamine depletion (ie. decompensation). In this setting the SNS activation via ketamine will be minimal while the myocardial depression may be pronounced.
Although I think it is fine to use ketamine in this situation I think that the physician must be aware that ketamine is a complex drug, and in this setting will likely cause hypotension.
Propofol will certainly cause hypotension and I would be reluctant to use it at all in this situation. If propofol is the only agent you have (ie. the only agent your anesthesia dept. says you are allowed to use) then remember that the dose requirements in patients with shock are much reduced. An initial dose of 0.25mg/kg would be a starting point, rather than the typical 1-2mg/kg. Propofol may precipitate PEA in this patient. If you really must use it I would also suggest delaying intubation, until large bore access is established, and the initial couple of units of pRBCs are in.
Finally I think fentanyl is a great agent in this setting, and every emerg has fentanyl. Fentanyl has a proven track record in hemodynamically difficult patients, particularly cardiac patients. As with other drugs the dose requirements are lower in a patient with a shock state. In a patient like this with profound shock you are probably looking at a slow bolus of 5mcg/kg before you will get optimal sedation for intubation (vs cardiac patients who may require 30+mcg/kg as initial dose). If I were using fentanyl I would also use roccuronium as part of my RSI. The fentanyl can be continued as an infusion to maintain sedation at a starting dose of 0.1mcg/kg/min. This is a single agent regime with fairly simple pharmacology, which in this patient I think is beneficial. It also allows the anesthetist the option of initially running the anesthetic as fentanyl TIVA, while continuing resuscitation, before adding volatiles (but I’ll let them decide that……if they don’t tell me how to do ED airways I won’t tell them how to pass the gas….).
Aaron
Ok. A few points to consider.
What does a central line add over a few big IVCs in the arms? Is it worth the time / risk in the first few hours?
As Aaron says this patient is on max adrenaline drive endogenously. So are vasopressors a good idea, or are you just making the numbers look good whilst ignoring the underlying pathophtsiology?
Any thoughts? Casey
Her Ph looks terrible but the resp acidosis component is readily reversible.
Acutely hyperkalaemia will be the killer especially if she is flooded with lots of red cells – this needs to be aggressively treated 20ml Calcium Gluconate 10% and HCO3 – mainly to assist the hyperkalaemia rather than the Ph (if you are not planning on intubating then HCO3 could make things worse), Insulin etc. Lab K results will lag behind the real serum K during rapid RBC infusions.
In a young person a HB of 58 is not terrible IF euvolaemic. The Hb obviously does not reflect the whole perfusion picture as her lactate is > 10.
She needs cautious volume replacement (RBC + N/ Saline) to restore volume, increase Hb but avoid giving excessive K. To avoid excessive initial resuscitation her BP should be supported by vasopressors.
Intubate after partial volume resuscitation to control CO2 and PH. Use anything but slowly and with 1/3 – 1/2 the usual doses
Obviously not Sux
Ventilate PaCO2 to low 20’s – high rate and low volume (not for lung protection but as better tolerated in volume depleted patients)
Surgery – saving her own RBC is better than giving K rich, O2 delivery poor pack cells. 5 minutes and a clamp will stop the bleeding
Despite her ABG I suspect she bounced back reasonably quickly
Casey is right, there is probably no drug that cannot be administered, at least temporarily, via a big proximal arm IVC and initial resus . The Hagen–Poiseuille equation tells us that the flow through an IVC is related to both diameter and length, so long central lines are generally disadvantageous in resuscitation.
Where I disagree with Casey is in the time issue. With US guidance I can have an 8Fr sheath in the IJ within a minute, much faster than the nurses are able to establish large peripheral IVs in a shocky shut down patient. I like a large sheath, you can pass a triple lumen through it, or change it out over a wire if you like as the case progresses, and initially it allows you to pour near limitless volume into the patient. Under ultrasound guidance the safety of placement is also much improved.
The use of vasopressors is a complex issue, We will need more clinical information from you to determine if the patient is in maximum adrenaline overdrive or if she has basically depleted all of her endogenous catecholamines in the 4 days she has been ill. If this patient still looks hyperadrenergic at presentation I think the pressor of choice is blood products. However, if she is no longer tachycardic, sweaty and anxious (which she should be) her sympathetic nervous system is also severely deranged and some use of vasoactive agents is probably going to be required as a bridge until by active resus she re-enters a physiological survivable milieux.
Aaron
This is turning into an epic thread – good stuff.
I was “trailing my coat” with comments on propofol and Cliff Reid – glad Aaron and Jonathon picked up on it. I reckon Cliff’s ‘propofol assassins’ rant should be played at start of shift to all anaesthetic registrars covering for trauma…
The “fully sick” RSI is a different beast to an elective case…ketamine or (I think) better still fentanyl would be a great way to go…
A propos central lines, it doesn’t take long to whack one in the IJV…I guess I am old school – learned 15 years ago in the UK. Under 90 seconds I reckon, unless you fanny around with USS… but whatever works for you. Big lines in big vessels is my mantra.
That said, peripheral access is perfectly acceptable – provided have dilated up to a 7-8Fr hosepipe with the RIC kit or used a Swan sheath…
Great thread. So, what happened next?
My Two cents worth:
As above:
Intubation/Induction
Yes she needs a tube but will a tube kill her?
What I am worried about is the induction killing the patient:
The First kill: Hypotension: Very small amt of induction agent consider fentanyl or ketamine or propofol. Lets face it what ever we are going to give is going to crash the pressure. A very small amt is going to be used no more then 2omg propofol, Fentanyl small amount ketamine.
Fluid Fluid Fluid !
Second Kill: Extreme Acidosis- The apnoea period is going to kill the patient 30 plus seconds! waiting for the Roc to work!
We need to think outside the RSI box. DO bag the patient during induction. IF you’re worried about the stomach insufflation try the vent as a bag using pressure control ventilation with 15mmHg (limited gastric insufflation) with a patent airway.
Do consider placing immediately a fasttrach or supreme. Can be placed rapidly and even better can with the supreme place a NG tube.
Third Kill: Hypoxia – Thankfully not an immediate issue
The other line to consider is IO.
1. Vasopressors are useful while the cause of the problem is address.
Increasing the numbers is exactly that. Improving perfusion pressure and blood flow distribution. I will accept potentially less total total blood flow for more regional blood flow to the head, heart and kidneys.
2. RSI
She is not at high risk of aspiration unless there are other details so why would you not ventilate her to control her CO2. Head elevation, (-/+ cricoid pressure), gentle bag mask with an oral airway and pressures under 15 and the aspiration risk is small.
The classic RSI is rarely indicated.
3. Drugs
Amnesia is the main aim so some midazolam is useful. But care must be taken with fentanyl and midazolam with delayed onset of action of 3 minutes causing hypercapnia. Alfentanil is better suited to the classic RSI.
Additional:
As stated above by all of us the tricky part here is the induction. Ketamine is a fantastic agent and it is my go to induction agent for most emergency RSI. However in this patient ketamine is likely to kill the patient esp in full induction doses this is going to absolutely crash the BP etc. This patients adrenals are working overtime. Propofol fantastic drug but once again in full induction doses = death. The trick is less is more get away with the bare minimum
Etomidate no experience with this agent as not licensed in Australia.
The controversial part is do we give a induction agent considering this is likely to kill the patient? I have thought maybe just using a very small amount of Midaz 0.5-1mg max, Fentanyl 20mcg just to block memory. The Other thing is the paralytic is going to take a while to work because the patient is shut down. So we need to wait a little longer and give more paralytic to get to work faster.
Patient needs Blood 1:1:1 ratio plus prothrominex. If we can whole blood even better (unlikely)
Lines whatever we can get in with the available resources that we have. If we have lots of hands that can simualtenously work ABC correction of the patient fantastic. If not I wouldn’t be going for a IJ straight away but go for IO.
The importance of communication skills. Cannot be underestimated. ensuring that every one knows what is going to occur the plans and declaring that this patient is critical and may die.
Casey you a magnet!
Hi folks and happy new year! What a case to start off with! I tend to agree with Aaron’s approach! About the Hyper K problem, did you repeat and double check the result on a venous spec to be sure? If genuine Hyper K then agree with what everyone else has said, but I would also bolus in hypertonic saline,3%,, it helps dilute the K as well as act as a volume expander..look it up there is some evidence to support its use in Hyper K and low Na. What about salbutamol, neb or IV? Works quicker than insulin to drive K intracellular.
Prob too late for TXA but I would give FFP whilst waiting for K to be corrected. Once K corrected can start transfusing PRBC.
FOr the emergency anaesthetic, RSI =really stupid idea, sux contraindicated, normal induction agents = PEA, aspiration risk prob not high assuming this is a first trimester problem, I have used fentanyl or similar based approaches here to great effect. Rocuronium is great if you got it but if not then vecuronium will do. Fentanyl and vecuronium timing of onset works about right. Whilst waiting for them to work, maintain oxygenation using nasal cannulae and applied BVM, genltle BVM ventilation to keep SaO up, I dont do cricoid any more in predicted low aspiration risk cases…so I would not even call this RSI..its intubation using a paralytic and opioid. Intriguingly if you have been following the debate on emcrit, regarding intubation without paralytic, you could do sedative alone intubation, or what Paul Mayo calls a graded sedative approach using vasopressor support. I would not use propofol though! A true legend of rural generalists, DR Peachey, tubed a guy who had shot himself in the face with a shotgun, using fentanyl alone and a bougie! opioid assistd intubation!
vascular access is needed but take what you can get! IO is fine initially but recent reports of amputations due to compartment syndrome after prolonged infusions via IO need to be heeded. Start your initial resus and operation but get central access as soon as practicable. PIV access is fine as well to start and if got RIC kit can convert a 20 G PIV into a short fat 10G catheter very quickly. But if Aaron is around and can get a cordis sheath into the IJV then I would be happy with that too!
I would be thinking this lady needs renal replacement therapy some time sooner rather than later, in particular if her Hyper K is genuine and due to pre renal failure. In other words, she needs to get to an ICU. Damage control type surgery may be needed here. Quick haemostatic surgery then into ICU for ongoing resuscitation and physiologic correction.