Clinical Case 096: Abdominal Ambiguity

Gday. Another quick case from the surgical files!  This is a diagnostic case that plays out intra-operatively. Put your thinking caps on – when does your “penny drop”?

This is probably more for the Anaesthesia types, but there is plenty in here for the ED docs and even surgeons out there.  Here we go:

46 year old man, a traveller – on his way around the north of Australia.  Usually fit and well, working miscellaneous manual-labour jobs to pay his way.

This chap had hitched a ride into town the day prior from a remote camping spot. He had noticed some “crampy belly pain” overnight – so thought he would pop into town for a check up….

At triage he reports: intermittent, central abdo pain that has become more right-sided and severe over the past 12 hours.  He is feeling “full”, not wanting to eat, vomited once en route this AM.  He gets a “cat 3” score, a bed and an IVC.  The triage note simply says: “46yo M, ?appendix

The trusty RMO gets the history – thin, well smoker.  Not much PMHx, had an inguinal hernia repair 20 years ago – otherwise a virgin abdo. No meds, no other chronic problems.

Obs:  T = 37.6, pulse = 100,  BP = 120/60  RR = 18/min  He is reporting a pain score of 7/10.   His pain settles with 10 mg of IV morphine.

On exam: tender over much of the lower abdo, right-side more than left.  Percussion tenderness at McBurnie’s point.

I heard about this case when the phone rang in theatre – I was doing an Anaesthesia list for the local Gynae.  The ED team were pretty sure he would get a look in OT and it was nearly sundown – so they wanted to let us know not to close up shop for the day!  The surgeon had been called to review in ED….

Ten minutes later we got a call form the Surgeon – he wanted to get this chap on the table tonight.  Now this was an old school surgeon – one that was happy to call it clinically.  No imaging or bloods required.  The story and exam did fit nicely with Appy, he was sore enough to suggest it was progressive and needed something doing.  So off to OT…

Yes hard to believe, I know! There are still places where surgeons operate without definitive imaging – they are fun places to work!

My Anaesthetic assessment was pretty dull – same as the ED notes.  Thin, fit, normal airway, looked like a dream tube.  Was still breathing up with a bit of pain in the holding bay.  The plan was for a “quick open appendix”.  Love the old school surgeons – no laparosopic adventuring when it is keeping us all out of bed!

Induction went well on 100 mcg fentanyl, 100 mg sux and enough propofol to do the trick.  Tube fell in easy and onto the vent….   now our first clue that something is awry.   The end-tidal CO2 on the first few vent cycles  comes back at 23 mmHg.

What does it mean?  We love the ET CO2 in Anesthesia-land.  You get A, B and C in a single squiggly line!

Airway is good – tube was easy, position check is OK, and we are seeing regular rise & fall of the CO2

Breathing seems OK – chest is moving well, the vent is happy with nice, skinny low pressures and we are reaching target volumes and a sensible MV.  SpO2 is 100% for what it is worth.  He was not bagged in the 25 seconds of apnoea…

Circulation – is the CO2 low because he has crappy output?    Nope – the BP is still 120/60,  pulse is 75 – hasn’t gone brady.  Looks like he is well perfused.  The volatile is washing in and he is peripherally flushed & pink.

So – why is the CO2 so low?  Sure he was breathing up pre-op… thought that was pain – nothing a slug of fentanyl shouldn’t fix???

Anyway – onwards – the Surgeon is true to form – he has cracked open the gridiron incision.  However, as he opens the peritoneum he starts to mutter…..  Occasionally we gas docs do wonder what it is that is going on down that end.  So I lean over the drapes for a gander – hmmm.  There is a good volume of haemoserous fluid pouring out of the incision – the scrub nurse is sucking it up, we are up to 300 mls before it starts to slow.  That is a bit odd – not the norm for an appendix – no pus, just lots of bloody serous fluid.

To make conversation (and try work out what the heck is going on) I ask: “Have you ever seen that before in appendicitis?”   There is no answer, just some brow furrowing.  Our surgeon is clearly deep in thought and is now looking for the offending appendage.

Meanwhile at the brain end of the room – the ET CO2 is falling now with relatively low volume ventilation – it is now 22 mmHg… and the BP is not looking so hot – that is down to 80/40 with a tachycardia developing 110/min.  So I do what Anesthetic folk do – a few boluses of metaraminol.  This seems to help the numbers.  Odd – he didn’t seem that sick or septic pre-op, yet he is behaving like one of those really nasty, peritoneal sepsis type appendix disasters on the table.  Reassured by a good heart and ‘young’ physiology I decide to wait & see what happens.

5 minutes later I peek over the drapes again.  Expecting to see an appendix with a few loops cast about it – I am disappointed to find the team preparing to open the midline.  A bigger cut, something is not right….
“Ahhemm! How is it going?”  I wonder.

The reply is along the lines of – well this is not appendicitis.  In true surgical form I am assured that we will know the diagnosis in a few minutes once the belly is properly opened.   Off I go looking for some longer acting paralytic – this is going to take a while!

OK.  SPOILER – I am about to reveal the diagnosis.  So take a moment to ponder your thoughts.  What else could be going on.  Not much to go on admittedly – as Vonnegut would say… “So it goes.”

About 4 metres of dead small boweldead gut.
 Suddenly the numbers all became clear – this was a seriously sick patient, compensating remarkably, but truly on the brink of collapse.

Time to change into the brown scrubs!  There is work to be done.

The CO2 was right all along – this is a guy with a good going metabolic acidosis, and a faltering cardiac output now thanks to my “routine RSI GA”.

First move – crank the ventilator.  We need to return the CO2 from whence it came – get that pH up ASAP.  But too much volume might kill the venous return – so I opted for a brisk RR and maintained ~ 6 ml/kg Vt.

Next – a big IVC, bolus of crystalloid.  I am a Hartman’s man when I am flying blind like this.  IS this the right thing to do?

I am not sure – the recent literature on fluid Resus and discussion in the FOAMed world has been controversial to say the least.  Is giving a big bolus going to do damage to this man’s fragile glycocalyx and lead to horrible organ failure win ICU in a few days?  Or is the Sevoflurane I am using going to protect his endothelium?  Should I use exogenous fluid bolus or use some pressors to squeeze the venous side and achieve the same ends?

I grab a VBG at the same time.  

pH = 7.05,  pO2 =40, pCO2 = 27, HCO3 = 10 BE = -12 Lactate = 7.7 Gluc = 8.0

It was at about this point I was recalling all the times I had derided the ED junior Docs for ordering all those “unnecessary” bloods and X-rays in the work up of belly pain.  Clearly this was the exception that proves the rule??

After a few litres of fluid – the BP is still pretty crappy and I have backed off on the volatile as much as I was comfortable.  I have used an amp of metaraminol by this stage – time to change plans.  I need to know what the heart is doing.  Is this an under filled heaving, healthy heart, or a sluggish poisoned pump?

So how does one go about making this call mid-operation.  Access is limited by the surgical drapes.  I can put a CVC into the IJ – but we all know that the CVP is a really silly number.  Still – it will be handy to run some pressors, and lets face it – this man is very likely going to a better place soon where he will certainly get one anyway!

Urine output…. a good thought.. but… there is no IDC in the bladder – this was going to be a quick in/out case.

So my plan of course involved ultrasound.  Instead of asking for the usual machine that lives in OT I really wanted the ECHO probe as well.

We do not have any fancy Cardiac Output monitoring devices – no oesophageal Doppler or USCOM etc.  However, in a thin guy on the table – a couple of parasternal ECHO views are usually achievable.  I reckon we can get an idea of the heart’s status with some reliability.  I am not suggesting we all do VTI and calculate the CO to 3 decimal places!  I just have an eyeball and say – is this heart hyperdynamic or underfilled, or is it hypodynamic.

Some information was forthcoming from my learned friend on the cutting side of the drapes – he noted that the ischemic bowel was full of haemoserous fluid – the mythical “3rd space”? There must have been 3 or 4 litres in what he was removing.

Unsurprisingly then the ECHO pics showed –  a really hyper dynamic heart with a collapsing LV – the EF was nearing 110%!  Ah – young patients – they can compensate so well without much to show on the surface!

OK – by the time the surgery was finished we had a 46 yo guy with a nasty ischemic gut.  He had lost about 75% of his small intestine.  An ileostomy was formed.

The metabolic acidosis had improved and I was able to wind back the vent a bit.  But the settings were :  RR 24, Vt = 440 ml with 5 of PEEP.  This was giving an ET CO2 of 33 and the latest ABG showed a pH of 7.25, lactate down to 3.1 and other numbers returning to normal.

He was loaded with opiates and ketamine and all the usual adjuncts for pain and nausea.

My question to you.  It is now 10 PM.  You are in a smallish hospital with no ICU.  The retrieval team have advised they won’t be there until after sunrise at best.

This is the dilemma – do you keep him tubed, ventilated and transfer to ICU tomorrow?  Or do you wake him up – run the risk he might hypoventilate and decompensate his acidosis in recovery… but free him from the potential downside of prolonged intubation etc.  Transferring him awake is much safer from the flight team’s perspective.

Oh – and why did he get dead gut.  Well I could tell you, but it would be more fun if you guessed – let me know your thoughts on the comments below!

Lots to discuss on this case.  Break your comments down into: Diagnostic, Biases / errors, Critique of my approach and Disposition.



  1. Wow Casey, what a neat case. You didn’t spoil it for me, by the way–your timing of “storytelling” is just about perfect. I have seen clinical scenarios like this with cases similar to these, and during ERCP’s. These patients are fine if you don’t touch them, and they decompensate when you handle their guts, either from the outside, or from the inside, as with an ERCP. Thoughts?
    1. Epinephrine infusion, 1-5 mcg/min not out of the question. Will not cause tachycardia in most people at that dose.
    2. Vasopressin infusion for sure.
    3. CVP introducer (if you have them)–they are great for volume infusion, and the tertiary hospital can use it for a swan if he needs it later. You also need CVP access for the vasoactive infusions, should you need any. IV infiltration of a peripheral IV with anything but Epinephrine will wreak hell on this patient.
    4. Fluid? We have albumin 5%. He needs a liter of it for sure–4 bottles of 250 ml each through a fluid warmer.
    5. Asleep or awake end of case? I am pretty line-happy with sick people–I would place an arterial line (with him still asleep) and let the numbers help me figure this out. CXR to check for lung effusions or pulmonary vascular congestion. If he experiences any stunning of the myocardium, due to the released toxins, he may have some heart failure symptoms. He is an easy airway, so extubation is not a huge issue. If he were a recognized (or unrecognized) difficult airway, the alone would make me keep him intubated and sedated overnight.
    6. So, here is my most concise answer:
    #1–Lines and Tubes: Aline, CVP, Surgeon may want to place G-tube to simplify postop care. Foley at end of case, with temperature monitoring if available.
    #2–Fluids–Your choice is correct, but I would give a liter of albumin to this guy.
    #3–If you keep him intubated, and you do not have an ICU, it may make more sense to handle the ventilation, sedation and monitoring by keeping him in the OR overnight, and use the inhalational anesthetic gases as the sedative. Your ICU is your operating room. Yes it would be unpleasant to stay there all night, but it is the most practical solution for your hospital–all the monitoring, ventilation and other gear is right there. Think Disaster Medicine in this approach.
    #4–I do not know why he has dead gut.

  2. Taylor Zhou says

    Ischemic gut may have been due to prev hernia operation – could have recurrent hernia and incarceration/strangulation, infectious (some diarrheal bug while camping?), adhesions. Unlikely embolic or malignant.

    I’d keep him intubated and sedated overnight. He may get sicker yet. I’m more concerned about hemodynamic instability and hypoxia/ARDS from sepsis than hypoventilation if extubated. I’d rather have the airway secured and gives me the option of paralyzing him if he starts becoming unstable.

    I don’t like using alpha-agonists as blood pressure support in sepsis, as that decreases cardiac output. RL/Hartmann’s is probably my first choice fluid as well. Surgeon made the right choice with ileostomy. Have seen primary anastomoses fall apart because of the tissue edema and vasoconstriction from pressors later that are necessary to deal with the septic shock.

  3. Gonna watch the comments evolve – but for now, emphasises the value of bedside USS in ED and POC lactate. Get ’em on any sick patient – you’d be amazed what they show before you commit to course of action…

  4. Jonathan Ramachenderan says

    Excellent case. This is exactly the type of predicament GP anaesthetists find ourselves in. No ICU, sick patient, middle of the night, thousands of kilometres to a tertiary hospital.

    Regarding the approach to the patient during the case. This my standard critical care approach.

    A: secured
    B: “crank the ventilator” as you did aiming for a ETCO2 >30
    C: Fluids (Hartmans will do), place an Arterial line (send a gas) and place a CVL in the RIJ (using an ultrasound) and start a noradrenaline infusion if needed, consider a Mg2+ 10mmol if the patient is having some runs of VT due to the toxic release of the ischaemic gut, I can’t do an echo just yet but would love to learn
    D: turn down the volatile, place a BIS (as Tim would say, random number generator), ensure good opioid analgesia with adjuncts if needed (ketamine), consider a BSL
    E: Measure the temperature, give antibiotics (piperacillin +tazobactam) will do
    F: make sure the electrolytes are under control. Check the K+ due to the acidosis

    So now what?

    We recently had a 80yo T2DM smoker with an ischaemic gut who the surgeons resected the ischaemic portion but still needed further surgery. She was hypotensive and acidotic needing CVS support. we transferred her intubated to Perth.

    In your situation, the acidosis is much improved and if the patient wasn’t requiring any haemodynamic support and was initiating breaths on pressure support, I would wake them up with this plan.

    A: extubate in theatre as usual but transfer to recovery with airway trolley next to patient ready to reintubate if required (easy tube remember?)
    B: place on 15L NRB then 6L/min, titrating to Sa02 and initial gas post extubation then check gas 1 hour after extubation to ensure the improvement of acidosis
    C: continue IVF, place an IDC to measure output, check Hb+, consider inotropes if BP starts to sag
    D: analgesia (PCA fentanyl), I wouldn’t use an infusion,
    E: continue antibiotics, measure temperature
    F: again check electrolytes and renal function to correct any abnormalities and early failure respectively
    G: ?why did the patient develop an ischaemic gut ? thrombophillia ? cancer ? infection ? strangulated hernia

    Of course Casey, in the same ABC vein of answering and supporting my decision to extubate, I would NOT extubate if:

    A: He was a difficult airway and I was worried about the need to reintubate
    B: metabolic acidosis was NOT improving/ developing ARDS
    C: Haemodynamically unstable requiring inotropic support

    I would be calling my wife and letting her know I wouldn’t be home anytime soon.

  5. If available I would use Plasmalyte or Albumin (plus electrolytes) as the IV fluid so that lactate can be better tracked.

    I’d also try to avoid adrenaline for the same reason, but in sepsis vasopressors like noradrenaline and vasopressin are more useful anyway.

    If you don’t have an US to gauge filling of the heart, you can use systolic pressure variation as a guide to systemic filling and venous return. Most open appendix patients will be positioned with arms out, so you should be able to put in a radial arterial line during the case.

  6. This is a fascinating case that would be a challenge for any anesthesiologist. Thanks for posting it–it’s much more relaxing to read about it without the time pressures and mental load of a real OR.

    I commend the resourcefulness of using focused TTE to answer a key clinical question and the willingness to consider “what might have been missed previously” in adapting to an evolving situation.

    Diagnostic: My top guesses in order are 1) mesenteric vein thrombosis (risk factors: intra-abd sepsis, smoking, possible undisclosed history of pancreatitis or portal hypertension), 2) volvulus of small bowel, 3) ischemic or embolic infarction.

    Comments on specific events: The workup and decision to proceed seem appropriate. (Hindsight has an area under the ROC of 1.0) This patient got what he ultimately needed most: a rapid trip to the OR.

    Assuming that the ETCO2 plateau was relatively flat (excluding obstructive airway disease as a significant contributor) the low value immediately after intubation is cause for concern. (Note that even with 30 sec apnea the rise is minimal.) Tachypnea (which may or may not be hyperventilation) at preop could be explained by either the fever or as compensation for decreased tidal volume (splinting). However, a low ETCO2 should raise a red flag for either decreased cardiac output (deadspace) or compensation for metabolic acidosis (true hyperventilation.) I would accordingly target an initial ETCO2 lower than “normal.”

    I agree with the choice of a balanced salt solution (Hartman’s/LR/Plasmalyte). Given the expected fluid infusion total, I would avoid NS. NS don’t match the expected composition of the sequestered fluid and will likely produce hyperchloremic acidosis. At some point I would add albumin to the fluid replacement regimen.

    It’s great that you could obtain a second IV; even with volatile agents, some profoundly hypovolemic are vasoconstricted . While doing that I would de-air the bag in place and infuse it under pressure.

    The rapid clearance of the lactate makes me wonder if the original elevated level reflected discrete bowel ischemia over generalized sepsis.

    Disposition: At the end of the case, in order I would 1) place an arterial line and send ABG, electrolytes, CBC, etc, 2) repeat focused TTE exam, 3) place CVC (in case condition later deteriorates and pressors/inotropes are needed, not for CVP monitoring). A urinary catheter can be placed at some point in all of that. Further decisions would depend on that assessment.

    I am less concerned about this patient being able to maintain metabolic compensation as it looks like he is making great strides there. However, I am concerned about generalized edema since massive fluid infusion seems likely. If he later requires ventilatory support, an airway that was “easy” only hours before (pre-resuscitation) can be a nightmare once he begins to resemble the Michelin man. While it’s speculation without the benefit of being able to examine the patient, short-term ventilation may not be the biggest threat to this patient. While I can’t offer expertise on patient transport, I can imagine both pros/cons to having the patient intubated.

    • Thanks Greg
      Great comments.
      For all intersested – the diagnosis was basically a large “loop” of gut becoming trapped under adhesions from the old hernia mesh repair. This must be uncommon so late after a mesh – but still it has to stay on the radar for any ? appendix in the non-virgin abdo.

      My guess is that if we had done a bedside US looking for an appendix in ED – it would have been obvious that there was something seriously wrong – lots of fluid filled loops tend to stand out on US, plus all that free fluid would have been detected. Another great reason to US if you can – it is part of the exam in my opinion.

  7. Very interesting case Casey….Something similar happened to me also sometimes ago…Cluster f****k case…I used similar approach but started earlier Norepi infusion via CVC..of course I had ICU bed available!!!!…I’m on the other side of the world but surgeons are the same everywhere!!!!!!……Why they Never comunicate with the Anaesthetist???!!!!

  8. Fantastic case Casey. Thanks for sharing. Reiterate as above that he received relatively urgent surgery which sounds like was exactly what he required.
    Retrospectoscope suggests benefits of a VBG in ED but admittedly most “barn door” appendixes don’t get one so can see why he didn’t. However your case may change my approach here.
    Share you concerns re use of IV fluids in sepsis/SIRS … have also reconsidered my practice given the paradigm shift in recent FOAM discussions on the topic, that I’ve discussed here:
    Cautious fluids, early norad probably wise. I wonder how easy fluid responsiveness can be assessed by passive leg raise in theatre and how happy the surgeon would be about it. Also do you have cardiac output monitors (we don’t yet in ED)? Alternatively as you discussed, echo would be useful here if skilled.

    One question: if he is 3rd spacing but then the 3rd space fluid is removed from the body by the surgeon … does that provide a greater justification for IV fluid volume compared with if the fluid was left in the 3rd space? As I’m feeling my way through this new fluid paradigm and the endothelial glycocalyx that was previously hidden to me, I’m really unsure.

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