Unresponsive Diabetic

[chbare]

Hmm...a few questions if I may?

What was the transport time to the nearest appropriate hospital? Were the EMT's able to effectively manage the airway with BLS techniques? I understand the pulse oximetry reading was 92% after placement on a NRB without the use of airway positioning or adjuncts?

I have a difficult time understanding why the EMT's opted to go with RSI even with several reliable indicators of a difficult airway? One one hand the patient has persistent trismus, while in another statement there is limited jaw movement and the EMT's are able to suction the airway. I am having a hard time getting a true picture of the patients actual airway situation.

While RSI is not contraindicated with the difficult airway, the person intubating must be confident and a double backup must be in place prior to going down that route. It seems that there was some discussion among the crew about performing the RSI? Were both members confident RSI was the proper route? Were alternative strategies discussed?

In addition, why was pulse oximetry not constantly monitored throughout the procedure. Were the EMT's able to provide effective BVM ventilations between intubation attempts and after the aborted attempt at placing the ETC?

I second the possibility of hyperkalemia r/t Succ admin. I understand the presenting rhythm was NSR; however, were the T waves Tall and pointed? During the RSI were any other changes noted other than sinus brady that went to asystole? Was a sine wave ever noted during the procedure?

Another possibility to consider would be beta blocker OD; however, the presenting rhythm was not bradycardia, and the bradycardia seemed to develop during the procedure.

Take care,

chbare.

[AnthonyM83]

Would it of note what he was originally in bed for? Illness? What kind? Any signs of sepsis or dehydration (I understand his BP was 150/82, but what is it normally without his meds). He's 81...does he get around much? Bed-ridden? PMH? Lung sounds?

Like others, was thinking bradycardia due to intubation attempts. I imagine the heart had also been under some stress with such a low BG level, so didn't handle intubation attempts well. I also wonder if something else could have set off a CVA (combination of blood clots and HTN from not taking meds?).

[triemal04]

Sorry this took so long. Think everyone pretty much got it. Just curious, did anyone consider prolonged hypoxia being a possible root cause of the problems? Vomit filled airway for an unknown amount of time ain't so good...

The lab results are listed below, but, even with what seems to be a pretty sick and unhealthy person in the best of times, I'm not so sure about the conclusion that's drawn about the cause of the renal failure. Anybody have any thoughts on that?

The patient received standard dosages of IV epinephrine and atropine while chest compressions and ventilations continued

After a short period of time, the patient regained palpable pulses. He began breathing on his own but was assisted with the BVM. Post resuscitation vital signs demonstrated a blood pressure of 210/110 mmHg, respirations 12

assisted, radial pulse 132. The monitor strip revealed a sinus tachycardia consistent with the pulse rate. No pulse oximetry value was documented. The mental status was unchanged.

The patient was transported to an emergency department (ED). He was later intubated in the ED. His condition didn't change while in the ED. A CT scan of the head and a chest X-ray were normal. He was taken to the ICU and underwent treatment with a hypothermia protocol.

While in the ICU, there was no improvement in mental status or any other clinical parameter. Twelve days after admission, life support was withdrawn at the request of the family. The patient later expired.

The cause of death was likely hypoxic encephalopathy complicated by prolonged hypoglycemia, which was the likely initial cause of the coma.

Discussion-

This was obviously a very sick patient. It's never a good prognostic sign when a patient has been obtunded for well over 24 hours. Further, when prolonged coma is accompanied by severe hypoglycemia -- suggesting persistent low blood sugar -- outcomes are not good.

Clearly, persistent and profound hypoglycemia has to be at the top of the list as a cause of this patient's coma. The fact that this patient didn't respond to a bolus of IV dextrose emphasizes the point. Although a second dose of dextrose might have been considered, this likely would not have made a difference since the glucose was only 93 mg/dL following the original administration.

The question is, what caused the fatal hypoglycemic event, and how might that bear on the RSI procedure decision?

Enroute airway treatment options were available in this case, as typically they're in most patients considered for RSI. Continued supplemental administration of oxygen via the non-rebreather with a nasal pharyngeal airway might have been sufficient. Nasotracheal intubation might have been successful.

RSI certainly was a reasonable, additional consideration -- at least in our system. However, this case presented two significant potential stumbling blocks. The first was the difficulty suspected on the pre-intubation assessment. This possibility was recognized by the crew.

Paramedics must evaluate their chance of success in these cases after an honest appreciation of their personal comfort and skills based on their training and experience. In other words, engaging in a difficult RSI may be reasonable for a highly experienced provider and not reasonable for a less-experienced paramedic. The treating provider in this case thought the intubation was achievable after careful evaluation. However, as the case played out, the estimation of a successful intubation proved to be incorrect.

In this particular patient situation, another and equally important risk in RSI relates to the likely explanation for the patient’s prolonged hypoglycemia; the very real probability of renal failure.

What are the clinical and historical risk factors suggesting renal failure in a patient who had never been dialyzed? The long-term presence of diabetes -- especially if poorly controlled -- may itself lead to at least kidney insufficiency, if not outright failure.

However, the most acute reason arguing for possible renal failure is the depressed level of consciousness and resultant immobilization for more than 24 hours. Obviously, the patient couldn't eat -- and most importantly -- wasn't taking any oral fluids. So, clinical dehydration was inevitable. Unfortunately, the crew made no comment on the hydration status.

As blood volume decreases, the amount of blood reaching the kidneys decrease and intense attempts by the body to conserve water and electrolytes occur. If the situation continues, renal function decreases quite rapidly.

In this case, it appeared the patient had been in one position in his bed for most of the time. As pressure increases in immobile muscles and tissues, cell breakdown occurs which releases myoglobin, as well as muscle enzymes into the blood. Myoglobin may clog portions of the kidney, further increasing the risk of failure.

As the kidneys begin to fail, many drugs aren't cleared efficiently from the body. This increases their duration of effects. Two drugs of importance in this case that likely weren't removed normally are metformin and glypizide -- the oral hypoglycemics the patient was prescribed. Additionally, in renal failure, the body's own insulin isn't cleared well -- adding to the risk of hypoglycemia. Persistence of the drug effects only complicated the fact that the patient was unable to take any oral source of glucose for at least 24 hours.

How does the high risk of renal failure affect RSI? This relates to the use of succinylcholine, which is a depolarizing paralytic agent. It is believed that succinylcholine raises serum potassium (K+) by about 0.5 mEq/L (normal serum K+ is approximately 4.0 mEq/L) during the process of inducing paralysis. Most patients, even with slightly elevated potassium levels, will tolerate a 0.5 mEq/L increase without difficulty. But if a patient's serum K+ is already high (for example at 7-8 mEq/L), a 0.5 mEq/L increase may result in acute cardiac decompensation -- related to dangerously high blood levels of potassium (hyperkalemia) -- and arrest.

Non-depolarizing paralytic agents (i.e. vecuronium, rocuronium) aren't associated with the complication of hyperkalemia. However, all non-depolarizing drugs induce a longer period of paralysis than succinylcholine -- and often aren't selected in the prehospital or ED environments for this reason.

The timing of this arrest, closely after succinylcholine administration, suggested a hyperkalemic arrest. The crew focused on the potential difficult airway problems in this case and did not consider the possibility of renal failure and elevated potassium. In fact, while RSI is a complex procedure, assessment of the risk of hyperkalemia is probably the most difficult part and the most readily forgotten aspect of the process.

In our system, we stress the evaluation for risk of renal failure. If the potential is recognized, RSI will likely be deferred. However, an option to obtain a 12-lead ECG to evaluate for cardiac changes consistent with hyperkalemia is available to crews, because we don't have the ability to measure serum K+ in the field. The ECG is by no means a perfect test, but if no apparent evidence of hyperkalemia is present on the cardiogram, RSI may be performed -- in a patient at potential risk of elevated serum potassium. In this case a 12-lead ECG wasn't done because the possibility of hyperkalemia wasn't considered.

Upon arrival at the ED, the following laboratory tests were obtained:

Serum bicarbonate level: 8 mEq/L (normal is approximately 25 mEq/L -- reflecting a severe metabolic acidosis -- pH 7.04

Serum Creatinine: 5.31 mg/dl (normal is approximately 1.

0 mg/dL, reflecting renal failure or insufficiency)

Serum K+: 5.4 mEq/L (normal is approximately 4.

0 mEq/L)

Review of the above laboratory values indicated the patient suffered from renal insufficiency -- if not renal failure. The serum potassium was elevated compared to normal but, as it turns out, not enough to cause the cardiac arrest.

Discussion of the events immediately prior to and during the arrest suggest the very prolonged hypoxia preceding EMS arrival along with hypoxia associated with the intubation attempt were most likely associated with the cardiac arrest.

Nevertheless, the risk factors for development of renal failure and/or hyperkalemia are under appreciated and should be considered by all providers using succinylcholine in an RSI protocol.

Be aware of the factors that may potentially prolong the effects of hypoglycemic agents (oral drugs and/or insulin). Situations such as dehydration, immobilization may worsen existing kidney disease or cause renal problems. In such cases, hypoglycemic symptoms will persist or recur shortly even after bolus with oral or IV glucose.

If available, ETCO2 capnography via nasal cannula should be used in respiratory distress cases. Capnography provides an additional objective assessment of the patient’s overall respiratory status, as well as the quality of ventilations.

Recognize that adequate airway assessments (what we term in our system as "patient selection") are critical prior to beginning intubation attempts – especially in RSI circumstances. Selection assessment determinations will sometimes lead to different choices depending on provider training and experience. Occasionally, an intubation may be either expectedly or unexpectedly more difficult after an adequate evaluation has been done. Familiarity and use of accepted backup airway devices -- beginning with the BVM -- is very important when this occurs.

Risk factors for hyperkalemia are likely under appreciated by RSI paramedics using succinylcholine. This is probably because encounters with renal insufficiency or failure patients being considered for RSI are very few in number. As a result, repeated emphasis and education for paramedics on this rare clinical reality, and its potential complications, is very important.

[AnthonyM83]

Cool case.

Thanks for posting it.

[firedoc5]

I agree with Scaramedic the most on this one. If field intubation was unsuccessful and ventilations required, why not good old fashion nasalpharyngeal airway along with oralpharnygeal airway if tolerated and BVM? (remember Iamb old school) Sometimes the old ways may be the best ways to fall back on, never forget that. At one time EOA was a possibility (if it's even being carried anymore). To me it seems like supporting each sign and symptom and it comes. May keep you busy and hope you have a even just a few extra hands. Just a duo coming into this sux, believe me from experience. Support what you can. I lost track, but I would have gave 50 amp gglucose Due to down time, I'd say there were multi-organ failure. Any aarguments Iamb open to any constructive criticism. I'm somewhat curious too.

[AZCEP]

Cardiac arrest following succinylcholine tends to happen a bit quicker than it did in this case. I'm not willing to hang it up as the cause, but it just doesn't fit too well for the scenario.

Hypoxia is definitely the most likely cause of the arrest. A trial of simple bag-mask ventilation might have given some information to suggest that RSI was a bad idea. I'd also wager that the providers did not consider the immobility of the patient as being a problem. 24 hours without moving allows muscle cells to begin atrophy. As they break down, they will leak potassium into the blood stream.

A little sugar, maybe some sedation, perhaps even nasal intubation, and transport. I'd have probably left the paralytics out altogether.

[akroeze]

I agree with Scaramedic the most on this one. If field intubation was unsuccessful and ventilations required, why not good old fashion nasalpharyngeal airway along with oralpharnygeal airway if tolerated and BVM? (remember Iamb old school) Sometimes the old ways may be the best ways to fall back on, never forget that. At one time EOA was a possibility (if it's even being carried anymore). To me it seems like supporting each sign and symptom and it comes. May keep you busy and hope you have a even just a few extra hands. Just a duo coming into this sux, believe me from experience. Support what you can. I lost track, but I would have gave 50 amp gglucose Due to down time, I'd say there were multi-organ failure. Any aarguments Iamb open to any constructive criticism. I'm somewhat curious too.

Hey doc5,

Don't take this the wrong way but had you consumed alcohol while posting? Posting while drunk is illegal in 49 out of 50 states.

I only ask because this seems a bit of an unusual post for you.

[akroeze]

Cardiac arrest following succinylcholine tends to happen a bit quicker than it did in this case. I'm not willing to hang it up as the cause, but it just doesn't fit too well for the scenario.

Hypoxia is definitely the most likely cause of the arrest. A trial of simple bag-mask ventilation might have given some information to suggest that RSI was a bad idea. I'd also wager that the providers did not consider the immobility of the patient as being a problem. 24 hours without moving allows muscle cells to begin atrophy. As they break down, they will leak potassium into the blood stream.

A little sugar, maybe some sedation, perhaps even nasal intubation, and transport. I'd have probably left the paralytics out altogether.

Immobility... thanks for pointing that out. That's one thing that I honestly hadn't even thought of. Out of curiosity, would you want to pretreat for that with bicarb and have other hyperkalemic 'antidotes' at the ready? Or is it more something to be aware of but not actively treat?

[chbare]

Pre-treatment for hyperkalemia would not be indicated unless you have evidence of cardiac conduction problems related to hyperkalemia. I would look for the typical ECG changes prior to considering giving medications. Typically, your serum potassium will have to be quite high before you start developing cardiac conduction abnormalities. (6 Meq/L or higher in my experience.) I can appreciate your thinking on this matter and having CaCl- and NAHCO3 within reach would not be a bad idea.

I would also expect a degree of Rhabdo in this patient. The risk of renal failure is a concern and fluid therapy if the patient can tolerate, would help "flush out" muscle death by-products and maintain renal perfusion. At some point, a foley cath will be needed as well. I know some people advocate NAHCO3 for Rhabdo; however, I really hesitate to administer bicarb without a better clinical picture. (Labs, etc)

Take care,

chbare.

[AZCEP]

With the presentation we were given, I'd choose not to perform RSI on this patient. Thus mitigating the hyperkalemic effects of succinylcholine.