April Case Of The Month

Title: Cardiac arrest during emergence followed by refractory hypoxemia, hypercarbia, hypotension, and rhabdomyolysis.

The hotline consultant received a call regarding a middle-aged large (>130 kg) male with a history of Type 2 diabetes and hypertension who suffered pelvic and lower extremity fractures following an MVA. Chronic medications included metoprolol and losartan. He underwent ORIF of a tibial fracture. He was induced with Propofol, relaxed with succinylcholine and subsequently vecuronium, and anesthesia was maintained with sevoflurane and fentanyl. The patient’s blood pressure, hemoglobin level, oxygenation, ventilation, temperature and end-tidal CO₂ were normal until the end of surgery. Despite discontinuing sevoflurane, the patient did not awaken. Blood glucose was 160 mg%. A brief period of moderate hypoxemia (SpO₂ >85%) was followed by a brief ventricular fibrillation arrest. Spontaneously circulation returned following IV epinephrine and before defibrillation could be performed. There was no evidence of emesis or aspiration during induction. CT scan was negative for epidural or subdural hematoma. The call from the ICU was 8 hours after the arrest, prompted by signs of refractory hypercarbia (PaCO₂ ~90 mm) despite delivered minute ventilation ~ 18 liter/min., tachycardia, PaO₂ <100 with FIO₂ 1.0 and PEEP 12 cm, temp ~39º C., and CK>20,000. The patient was on a vecuronium infusion, and no rigidity was noted. He was on multiple pressors/inotropes for treatment of hypotension. The patient was now anuric. Serum potassium level was 6.3 mEq/L.

The caller asked 1) could this be postoperative MH? and 2) even if not MH, could dantrolene be beneficial by reducing CO₂ production?

1) What additional standard OR monitor would help you distinguish which process underlies the observed severe hypercarbia despite increased minute ventilation?

2) In general (not limited to this case), which of the following are potential causes of hypercarbia?

a) Decreased minute ventilation

b) Increased carbon dioxide production

c) Absorption of insufflated carbon dioxide

d) Incompetent unidirectional valves in a breathing circuit

e) Increased dead space ventilation

f) Bypass of carbon dioxide absorbent

g) ALL of the above

3) True or False: Endobronchial (i.e. right mainstem) intubation usually results in hypercarbia

The end-tidal CO₂ was <30 when the PaCO₂ was 90.

4) True or False: The large arterial to end-tidal CO₂ gradient indicates greatly increased dead space ventilation and inadequate alveolar ventilation.

5) True or False: Increased dead space ventilation is seen only with pulmonary embolism.

6) The brief episode of ventricular fibrillation was most likely caused by:

a. acute coronary thrombosis

b. hemorrhagic shock

c. hyperkalemia

d. fat embolism

7) The patient’s muscle tone is flaccid on the vecuronium infusion. Do you anticipate that dantrolene will significantly reduce muscle metabolic rate?

a. yes

b. no

Transthoracic Echocardiogram showed right ventricular dilatation and poor contractility, shift of the interventricular septum with reduced left ventricular filling. Nitric oxide was used to try and improve pulmonary blood flow. The patient did not survive despite strenuous efforts to optimize ventilation, support cardiac function, treat hyperkalemia and initiate dialysis.

Answers

Capnography, measurement of end-tidal and inspiratory carbon dioxide.
g
False
True
False
d
No

Narrative: This patient with pelvic and lower extremity fractures had been hemodynamically stable until emergence from general anesthesia. There was no unanticipated hypercarbia during surgery. This excludes MH as the cause of the cardiac arrest during emergence. The initial lack of awakening followed by hypoxemia and subsequent ARDS (acute respiratory distress syndrome) support a diagnosis of fulminant fat embolism syndrome. It is unlikely that a acute coronary thrombosis caused the brief V Fib arrest, given the prompt return of spontaneous circulation without defibrillation. Lack of preceding hypotension and recovery without specific treatment for hyperkalemia exclude hemorrhagic shock or hyperkalemia as causes of the initial cardiac arrest.

Hypercarbia is usually due to one of the following:

1) inadequate minute ventilation

2) pathologic dead space ventilation despite normal or increased minute ventilation, resulting in inadequate alveolar ventilation

Increased carbon dioxide production is a much less common cause of hypercarbia. It may be due to a benign cause, such as increased carbohydrate metabolism with total parenteral nutrition, or due to a rare, potentially life-threatening MH crisis.

In the operating room, other potential causes include equipment malfunction (e.g. incompetent unidirectional valves or ineffective CO₂ absorption), usually marked by an increase in inspired CO₂ level, or a complication of laparoscopic CO₂ insufflation. Endobronchial intubation does not typically result in hypercarbia unless diminished compliance results in reduced minute ventilation.

The huge increase in arterial to end-tidal carbon dioxide showed that dead space ventilation was massively increased. While we typically associate embolic phenomena (thrombus, air, fat, or amniotic fluid) with increased dead space ventilation, any process that reduces pulmonary blood flow will increase dead space ventilation, including cardiac arrest or acute hemorrhage. Despite an increased minute ventilation, this patient’s alveolar ventilation was reduced.

Dantrolene decreases skeletal muscle metabolism by reducing calcium release from the sarcoplasmic reticulum. The consultant thought it was unlikely to significantly reduce carbon dioxide production in a patient with flaccid muscle tone following vecuronium.

Fat embolism is characterized by hypoxemia with dyspnea, CNS depression disproportionate to the degree of hypoxemia, and a petechial rash. Skin biopsy of the rash may demonstrate intravascular fat. The incidence may be 5-10% in patients with multiple fractures. It may occur during spinal or epidural anesthesia as well as general anesthesia, or may occur during the postoperative period. Supportive care focuses on treatment of hypoxemia or ARDS, and precautions in a patient with depressed mental status. The prophylactic use of corticosteroids may reduce the incidence of fat embolism syndrome, but there is no evidence for therapeutic benefit. There are a few case reports of patient survival with use of ECMO, sometimes termed PCPS (percutaneous cardiopulmonary support), in cases with fulminant ARDS and right ventricular failure.

General Reference on Fat Embolism:

Glazer J. JABFP 2001; 14: 310-313

Prophylactic use of corticosteroids:

Cavallazzi. J Bras Pneumol 2008; 34: 34-41

Use of ECMO in treatment of fulminant fat embolism syndrome:

Igarishi et al. Br J Anaesth 2006; 96:213-215

Arai et al. Anesthesiology 2007 ; 107 : 509-511

Harvey Rosenbaum, MD

UCLA

Los Angeles, CA