Confusion and Dyspnea in the Dialysis Patient

A 67 year-old man with history of COPD, HIV (CD4 50), peripheral vascular disease, DVT, and chronic renal failure presented to the ED with AMS and dyspnea after missing one dialysis session due to a transportation issue. His home attendant found him at home confused and called EMS. She reported that there was no recent fever, chest pain, abdominal pain, nausea or vomiting. The patient was recently hospitalized for 2 days due to a COPD exacerbation.


BP: 156/66. HR: 81. RR: 22. Temp: 97 POx: 100% on O2 at 2 L/min.

Appearance: Lethargy; responsive to pain.

Eyes: Mild left conjunctival injection.

HEENT: Atraumatic

Neck: No JVD

CVS: Normal heart rate and rhythm; heart sounds normal; pulses normal. Dialysis catheter present in L chest wall.

Respiratory: Mild respiratory distress; shallow respirations; mild end-expiratory wheezes.

Abdomen: Soft and nontender.

Skin: Skin warm and dry; normal skin color; no rash; normal skin turgor.

Extremities: RLE BKA; no signficant LE edema; RUE with mild edema.

Neuro: Generalized weakness.

ECG: NSR, normal axis, prolonged PR, QRS 140ms, Peaked T

Bedside sonogram: A lines present, no B lines, good contractility, minimally collapsible IVC

Venous blood gas:
pH 7.0
K 8.5
CO2 100
HCO3 21
Hct 39
Lact 0.6

BUN 103
crn 11.8
trop 0.03

I know that you all know how to treat severe hyperkalemia. Calcium gluconate 2g, dextrose 50g/insulin 10u, and albuterol 20mg were given. 2 hours after arrival, hemodialysis was started in the ED. Ipratroprium 0.5mg, dexamethasone 12mg, and broad-spectrum antibiotics were also given. A critical care medicine consult was sought, and the fellow insisted on intubation and mechanical ventilation. She also reported that there were no ICU beds available and asked for the obligatory ABG.

1) Will doing the requested ABG assist in the immediate management of this patient? If so, how?

2) Would you follow the recommendations of the “consult” and intubate this patient? If so, which ventilation settings would you use? If not, then what alternative therapies would you employ (be as specific as possible)?

3) What type of respiratory insufficiency is present (Type I or Type 2)? What are possible etiologies of this patient’s respiratory insufficiency?

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Ian deSouza

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5 comments for “Confusion and Dyspnea in the Dialysis Patient

  1. wendyrollerblADES
    October 1, 2016 at 5:44 pm

    Doing an ABG will not change the immediate management, however an ABG is the only accurate measurement of hypercarbia and for trending hypercarbia (IE pre and post intervention). This patient is altered and mildly tachypneic with hypercarbia vs uremic encephalopathy vs infection being the likely etiologies. The decision to place on mechanical ventilation is ultimately clinical, to be guided in part by lab values. There is no firm cut-off for CO2 requiring intubation nor signs of fatigue or altered mental status interfering with oxygen delivery therapy in this case presentation so the choice of intubation should be left to the attending provider. Personally I would do a trial of Bipap because intubation in an asthmatic or COPD patient has risks including autopeep “breath stacking” which could lead to hemodynamic collapse. While there is promising data for high flow nasal cannula in acute hypoxemic respiratory failure,, there are no large trials demonstrating a benefit in hypercarbic patients. In the hypothetical hypercabic AMS patient who is hypovenilating, intubation should focus on maintaining a prolonged expiratory phase, I:E ratio 1:4 with a tidal volume of no more than 8ml/kg. Finally regarding treatment, this patient should be dialyzed STAT. This will significantly improve the available lung parenchyma for gas exchange. This patient has acute on chronic respiratory acidosis and a metabolic acidosis. (acute met acidosis with compensation would have a hc03 of 30, chronic would be 48?!) This patient has type 2 respiratory failure, secondary to COPD vs fluid overload.

    • Ian deSouza
      October 4, 2016 at 2:32 pm

      Good answers! Just to reiterate, in the vignette, the patient is currently receiving dialysis. Also, the bedside US did not reveal B lines therefore strongly suggesting the absence of pulmonary edema.

  2. dzeccola
    October 4, 2016 at 2:20 pm


    1) What is an ABG gonna tell us that the VBG or Chem 12 hasn’t. That he is hypercarbic? We know that already. That he has acidosis. We know that too. His acidosis probably isn’t from missing one dialysis session. The acidosis is from his CO2. If you remember that annoying henderson hasselbach equation we expect a drop in pH = 0.08 x (PaCO2 – 40). In his case that’s 60 x 0.08 = 4.8. That means with that CO2 his expected pH is <7.0! Remarkably, in spite of his renal failure he's showing some metabolic compensation. I've had some situations were well meaning but wrong consultants will ask you to give bicarb at this pH, and potentially this consultant is thinking of that when asking for a "more accurate" pH on the ABG (they correlate fine). That would probably be a "game over" move here. Bicarb works to lower serum (H+) by combining the HCO3- ion with H+ to make CO2 and H20. In a patient that is breathing, the CO2 leaves via the lungs and all is hunkey dorey. What happens if you already can't get rid of CO2? Well CO2 is even more able to cross cell membranes than H+, so now we have worsening CO2 levels diffusing across cell membranes leading to worsening intracellular acidosis and you guessed it, death. So short answer: I don't see any new information I can get from an ABG.

    2) Intubate. Why do we intubate people? a) because they don't have or can't protect their airway. b) they arn't breathing anymore c) because we can't push enough gas through a bipap mask to pop open alveoli to maintain some degree of normoxemia. Is there anything wrong with this guys airway? well, maybe, the stem doesn't really give us enough info on this one. People can get so Narced out on their own CO2 that they can no longer keep their mouth open/vomit out of their airway. So I might have to say "i need more info" on that one. Is he breathing? RR 22. Seems a bit weak to me given a CO2 of 100, nevertheless, lets remember this guy is a chronic CO2 retainer, and might have lost his chemosensitivity to hypercarbia. I would turn down the O2 and let that sat sink to 88-92% and see if he breaths any faster before I made this decision as well. If his sat is 88 and he is still breathing a paltry 22, It might be time to start breathing for him. And lastly he doesn't seem to have an oxygenation issue so no indication there. All of this is moot though if you havn't tried NIPPV, assuming he's get even a whiff of mental status. That will reduce CO2, reduce work of breathing ( a little). I would choose a low O2 (30%?) and an inverse I:E ration. Back to the question. Generally, don't like intubating people. I remember too many folks i've intubated and the conversations we had were the last ones they ever had with anybody. Sometimes it was inevitable, but other times it was a judgement call, and if someone is going to die, you might as well let them talk with their family while they're doing it. Intubating this guy is gonna mean possibly some apnea time. When your pH is already 7.0 from your CO2 of 100, you've got ZERO room for that to get worse before he goes into an arrhythmia from that acidosis. If i DID had to intubate this guy for any of the above reasons. I'd probably do an awake intubation with ketamine alone and then I would put him at a RR of 30 with an inverse I:E ratio and a TV of probably 7 ml / kg. I'd give him a bunch of fentanyl/propofol so that he could tolerate the I:E reversal without needing paralytics.

    3). This is type 2 failure. Why? Probably COPD? Sorry, I don't have a long winded answer on that one.

    • dzeccola
      October 5, 2016 at 11:02 am

      Forgot to mention, regarding intubation meds, if that is necessary, what happens when you give a patient with a K+ of 8.5 succinylcholine? We may laugh at them but theres a reason Anesthesia asks us for the K+, it can raise the serum K by another 0.5 meq/L. Just saying.

  3. Ian deSouza
    October 13, 2016 at 1:20 am

    Great answers and additional points from you both. Here is the case conclusion:

    The decision was made to try non-invasive ventilation because the thought was that respiratory function may improve with hemodialysis. The patient was placed on bilevel positive airway pressure and needed IPAP 24/EPAP 8 RR 16 in order to achieve a maximum TV of around 300-350. (See figure 1, Davidson AC, et al. Thorax 2016;71:ii1–ii35. doi:10.1136/thoraxjnl-2015-208209). He also needed regular reassessment for repositioning of his airway and adjustment of the BiPAP settings.

    Over 3 hours, serial ABG demonstrated improvement in pH and CO2 (116 to 103). Most notably, the patient’s mental status began to rapidly improve and his TV increased. He was able to mumble answers to simple questions. Once dialysis was completed, the nurse came and asked if the patient could walk to the bathroom to move his bowels. And gloriously, he did so. (This was followed by a short, uneventful inpatient course.)

    We cannot know for sure, but since the patient clinically improved so rapidly with dialysis, it is likely that the type II respiratory insufficiency was exacerbated by diaphragmatic weakness due to severe hyperkalemia. There are case reports of this phenomenon, one of which describes a “hyperkalemic paralysis resembling Guillain-Barre Syndrome”.

    Livingstone IR, dimming WJK. Hyperkalaemic paralysis resembling Guillain-Barri syndrome. Lancet 1979; 2: 963-964.

    Barker GL. Hyperkalaemia presenting as ventilatory failure. Anaesthesia 1980; 35: 885-886.

    Freeman SJ, Fale a D. Muscular paralysis and ventilatory failure caused by hyperkalaemia. Br J Anaesth. 1993;70(2):226-227.

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