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Failed RSI in a Comatose Patient


EMS crews were dispatched to the home of an 81-year-old male. His sister found him lying on a bed. When he didn't respond to her, 9-1-1 was contacted. He had complained to friends that he hadn't been feeling well for three to four days, and neighbors who had periodically checked on him thought he was sleeping for more than 24 hours.

Upon arrival, the crew noted the patient to be unconscious with snoring respirations. The past medical history included non-insulin dependant diabetes and hypertension. Medications included metformin and glipizide, as well as an unspecified beta blocker for hypertension. According to the sister and friends, the patient hadn't expressed any suicidal ideations and didn't possess a Do Not Resuscitate (DNR) order of any type.

Physical assessment of the man demonstrated obvious coma with persistent trismus. Copious amounts of emesis were present in the mouth and on the face. The initial vital signs included a heart rate of 89 beats per minute, blood pressure 150/82 mmHg and respirations of 24 per minute. The cardiac monitor demonstrated a sinus rhythm at a rate consistent with the pulse. Room air oxygen saturation was 82%. No end-tidal carbon dioxide (ETCO2) value was obtained prior to intubation attempts. The Glasgow Coma Scale (GCS) was estimated to be 3. The remainder of the physical examination was reported to be unremarkable.

Oxygen at 15 liters via non-rebreather mask was placed with improvement in oxygen saturation to 92%. Blood sugar determination revealed a value of 20 milligrams per deciliter (mg/dL). After an IV line was successfully placed, the patient received 25 grams of dextrose. The follow-up blood sugar was 93 mg/dL. No improvement in mentation was noted.

Given the patient's continued coma and apparent inability to protect the airway, consideration was given to Rapid Sequence Intubation (RSI) by EMS personnel. The pre-intubation airway assessment suggested the possibility of a difficult airway. The patient was noted to be obese. The neck seemed short and there was limited mouth opening to work with. The crew discussed these factors and, after some debate, elected to proceed. No 12-lead ECG was obtained prior to beginning the RSI.

The estimated weight was 110 kg. The patient was given appropriate dosages of etomidate and succinylcholine. Adequate paralysis was achieved. One attempt to intubate was made but was unsuccessful. During this time the head was repositioned and a bougie was utilized, but neither helped.

The patient was ventilated with a bag-valve-mask (BVM) and was suctioned. It was decided to place a Combitube. But this device was not able to be inserted far enough into the mouth and was ultimately abandoned.

Vital signs at this point were documented to consist of a blood pressure of 190/112 mmHg, respirations 12 per minute assisted, and a pulse rate of 48 beats per minute. Sinus bradycardia was seen on the monitor. No pulse oximetry value was recorded at this time. An oral airway was inserted, and the patient was continued on the BVM.

The patient rapidly became more bradycardic and then developed asystole on the monitor. No pulses could be palpated.

CPR was initiated.

What do you think might be causes for the patient's coma?

How would you have treated this patient?

What do you think might have caused this patient to go into cardiac arrest?


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 Intensive Care Unit (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.


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.

What can we learn from this case?

  • 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. I am always concerned about these factors when I consider a refusal related to a hypoglycemic patient who appears to have been successfully treated in the field. I always ask the crew details about the clinical circumstances searching for possible renal insufficiency or failure risks. Additionally, I ask the crew to fully describe the medications the patient is taking for diabetes along with dosages and most recent use, as well as the patient s ability for oral intake. I put all of these factors together, along with whether another party will be accessible to the patient, when evaluating a refusal request. I suggest that EMS providers have this detailed information available when contacting medical control regarding refusals for treated hypoglycemia patients.
  • 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.


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