July Case Of The Month

 

Hypermetabolism and Robot-Assisted Laparoscopic Surgery

 

            An 82 kg, 5 foot six inch, 46 year old Caucasian woman was scheduled for robot-assisted laparoscopic resection of uterine fibroids, possible hysterectomy. Her past medical history was significant for several uncomplicated prior surgeries under general anesthesia and a recent near cardiac arrest in the Emergency Department that was associated with profound anemia attributed to dysfunctional uterine bleeding.

            On the morning of surgery, IV sedation was provided with midazolam and fentanyl prior to a lidocaine/propofol IV induction. Following demonstration of an adequate mask airway, intubation with a 7.5 ID cuffed orotracheal tube was facilitated by 100 mg rocuronium and anesthesia was maintained through a semi-closed circle system with 1.8% sevoflurane in oxygen with a 3 L/min fresh gas flow. An orogastric tube was passed and confirmed to be in the stomach by auscultation. A bite block and esophageal stethascope were positioned as a second IV was placed for venous access.

            During initial surgical preparation and positioning, the HR was observed to increase from 80-90 bpm to 110-120 and increasing PETCO2 led the anesthesia team to increase ventilation progressively to 15 bpm X 1000 ml. As the PETCO2 on these ventilator settings was 46 torr and an increase in esophageal temperature to 99.8° F was noted prior to abdominal incision and trochar insertion for CO2 insufflation, an arterial blood gas was obtained.

Questions:

 

1)                  What is the diagnosis?

a.       Definite MH Crisis

b.      Possible MH Crisis

c.       Inadequate Ventilation

d.      Light Anesthesia

e.       Unknown Hypermetabolic State

 

2)                  What would be your first priority?

a.       Verify effective ventilation

b.      Increase anesthesia concentration

c.       Initiate BIS monitoring

d.      Delay Surgery/CO2 insufflation pending ABG results

 

            Arterial blood gas report was called into the OR with the following:

pH = 7.23, pa02 = 248, and paCO2 = 54. The serum K+ was 5.4.

 

3)                  This picture is most compatible with?

a.       Inadequate Ventilation

b.      Hypoperfusion and Acidemia

c.       Hypermetabolism

d.      Acidemia due to mixed metabolic and respiratory processes

 

4)                  The safest clinical plan at this time would be to?

a.       Place an arterial catheter for serial blood gas and electrolyte monitoring and continue with surgery after increasing ventilation and administering 2 amps bicarb.

b.      Increase ventilation, administer bicarb. and continue surgery with close monitoring and use non-MH triggering agents for anesthesia.

c.       Delay or cancel surgery, treat metabolic disturbances and monitor patient.

d.      Cancel surgery, increase fresh gas flow, discontinue sevoflurane, administer dantrolene sodium 1-2 mg/kg, increase ventilation using an alternate ventilatory source, administer bicarb., fluid challenge with cooled 0.9 N. saline, place an arterial catheter for serial blood gas monitoring, and call the MH Hotline.

 

            Surgery was cancelled, anesthesia was discontinued, the patient was uncovered and exposed to the cold OR, 2 amps of sodium bicarbonate and a fluid bolus were given, an arterial catheter was placed for serial blood gas monitoring, and a repeat blood gas with CBC and serum electrolytes were obtained. During this time the esophageal temperature decreased to 99.2°F, the HR to 108, and the PETCO2 to 32 torr on the settings noted above. A repeat ABG showed the pH had increased to 7.32 with the paCO2 = 38. Serum K+ was 4.9. A call was made to the MH Hotline. Over time it was noted that this intubated patient was awakening with stable vital signs, declining heart rate, a more normal temperature, and no tachypna. The urine was not discolored.

 

5)                  If you were the MH consultant called to advise the anesthesiologist at this time, what would you recommend?

a.       This is a classical MH crisis, administer dantrolene immediately.

b.      It was wrong to cancel surgery.

c.       The underlying process is obviously an infection.

d.      This is an unknown adverse metabolic reaction associated with anesthesia like that seen in MH, with an undiagnosed muscular disease,  or some other drug reaction and requires close monitoring and supportive therapy.

 

6)                  In this setting, important supportive therapy may include:

a.       Pharmacologic control of acidosis and hyperkalemia.

b.      Continued mechanical ventilation.

c.       Sedation for control of anxiety and agitation.

d.      Antipyretic therapy with drugs, topical and IV cooling.

e.       Administration of Dantrolene.

f.        Diuresis and Alkalinization of the Urine.

 

            During the next 24 hours the patient was extubated with normal vital signs and had no complaints. ABG, electrolytes and urine were normal. The CPK was initially elevated to 4,000, peaked at 18,000 by 14 hours post-event and returned to normal. Serum electrolytes, BUN & Creatinine were within normal limits. Myoglobinuria was never documented.

 

7)                  This clinical course is compatable with:

a.       Malignant hyperthermia.

b.      A myotonic crisis.

c.       Gentamicin toxicity.

d.      Urosepsis associated with urinary catheterization.

 

8)                  Should this patient be treated as though she is MH susceptible when she has her urgent abdominal surgery?

a.       No, close monitoring only is indicated, since we don’t know the diagnosis and can treat MH if it occurs.

b.      Yes, she should not have surgery. She should only have local anesthesia or sedation until this issue is resolved.

c.       Yes, she will inevitably need surgery for control of bleeding and the safest approach would be to treat her as MHS, avoiding MH triggering agents, while monitoring her closely.

 

Answers

1)      This presentation is remarkable for the rapidity of it’s evolution. The anesthesia team observed tachycardia associated with presumptive hypercapnea despite a minute ventilation that appears to be > 2 times that predicted. It could reflect ventilatory problems like rebreathing in a damaged anesthesia circuit or with an exhausted carbon dioxide absorber. An unexpected drug reaction or underlying septic process might also be causes. An evolving MH crisis or adverse metabolic process associated with an undiagnosed underlying muscle abnormality are also possible. The best answer is “e”, unknown.

2)      While an immediate concern is to verify that there’s nothing wrong with the airway, the anesthesia circuit, or the mechanical ventilator, manual ventilation should have confirmed that the seal is adequate, fresh gas flow also should be increased to overcome any occult rebreathing. Verification of effective and adequate ventilation should have taken place concomitantly with the appreciation of an increased minute ventilation requirement. Whatever the cause, it is a signal to slow down the surgical process and obtain an ABG. Within a very short period of time, results of an ABG can clarify whether surgery can continue safely or delayed for further investigation. Assuming that the problem is “light anesthesia” could be very dangerous because it can delay definitive therapy when there is an unexpected hypermetabolic crisis like MH. The BEST answer is that the first priority is to obtain independent confirmation of the adequacy of ventilation that will rule out other issues.

3)      The blood gas documents academia associated with hypercapnea and metabolic acidosis. In the clinical setting of an unexpected, marked increase in ventilatory requirement together with tachycardia and an evolving fever, this must be a hypermetabolic problem causing relative hypoperfusion and hypoventilation.

4)      Choices “a” & “b” are unwise. Choice “c” is adequate only if close monitoring demonstrates resolution of the process with supportive therapy and anesthetic withdrawal. The “d” choice is safest because it initiates early therapy for one of the most dangerous of the hypermetabolic possibilities while supporting the patient’s circulatory and metabolic needs and discontinuing possible triggering agents. Dantrolene may be life saving, if given soon enough in this setting. Possible side-effects are less critical. The balance of risk favors assumption that this patient may be experiencing an MH crisis.

5)      The clinical evidence presented suggests slow reversal with supportive therapy of whatever this  hypermetabolic process was, but the process is still unknown and may be associated with critical secondary insults to the kidneys and other organ systems. While surgery is clearly indicated by this patient’s DUB, there is time to stabilize and monitor the patient.

6)      Depending on the clinical course and subsequent data all of the listed supportive therapies may be indicated. During the phone conference with a MH Hotline consultant, it was evident that circulatory and respiratory requirements were normalized with resolution of fever and hyperkalemia. At this time the primary concern was to rule out other processes and follow the patient for occult rhabdomyolysis, coagulopathy, encephalopathy, myocardial or pulmonary injury and other significant consequences of an unknown hypermetabolic event. Close clinical and laboratory monitoring is the only way to identify supportive therapies that may be necessary. Absence of findings like fever and obvious rhabdomyolysis don’t preclude recurrance or evolution of these processes. In the anesthetic setting MH and occult muscle disease-associated crises can cause rhabdomyolysis and delayed renal failure. Consequently “f” should be implemented if there is any evidence of myoglobinemia— dark, concentrated urine that with a positive dipstick indicator for hemoglobin and, later, a positive urine or serum myoglobin measurement— while maintenance of good urine output with fluids is relatively benign and protective while these tests are obtained.

7)      Given laboratory evidence of normal renal function, the serum CK elevation observed and time course confirm a significant muscle insult with cell death. Initial CK elevation suggests this was immediately and temporally associated with events in the OR. Careful neuromuscular evaluation should eliminate occult muscular dystrophy, central core or other rare muscle diseases from the etiology. A self-limited MH crisis is the likely prospect for a woman of this age with a negative personal and family history. Both contracture testing and genetic studies would provide useful information for her, her doctors, and her relatives. This can be achieved through a biopsy center director for referral and counseling. Information about the Adverse Metabolic Reaction to Anesthesia report, contracture testing referral, and genetic testing is available on the MHAUS web site (http://www.mhaus.org).

8)      It is unrealistic to deny someone urgent surgery and propose multiple transfusions while an ideal work-up is completed. If a near cardiac arrest associated with anemia caused by DUB isn’t an indication for definitive GYN surgery, what is? While the patients diagnosis is not definite, the significant rhabdomyolysis and peri-anesthetic hypermetabolism she experienced suggests that anyone who exposes her to triggering agents is exposing her to a high risk of a worse recurrance.

Charles B. Watson, MD, FCCM
Chirman Department of Anesthesia
Bridgeport Hospital
Bridgeport, CT