Fig. 11.1
Effects of a sudden increase of the pulmonary artery pressure on the cardiac ejection fraction
The exact cause of the reaction to the cement is not fully understood. In the past, the monomer particles were thought to have direct cardiotoxic effects, when washed into the circulatory system. This theory is now believed to be unlikely. It is now known that MMA monomers stimulate the release of anaphylatoxins C3a and C5a, which cause histamine-mediated allergic reaction. To prevent this reaction, some authors recommend histamine blockade [8].
The most important trigger for a Palacos® cement reaction is probably pulmonary emboli. By using TEE in patients undergoing hybrid prosthesis surgery, 61.5 % of the patients were found to have had serious pulmonary emboli [5]. The observed micro- and macroemboli could have consisted of air, thromboembolus material, fatty bone marrow, or cement particles.
The result is acute increase of the pulmonary arterial resistance and the intrapulmonary shunt. Since the ejection fraction of the right side of the heart is tightly dependent on the myocardial filling pressure (Frank Starling Mechanism), the observed arterial blood pressure decreases are more severe when any of the following takes place:
A volume deficit is present
The ventricular filling mechanism – for example, in atrial fibrillation – is impaired
The right-sided ventricular function is impaired
The extent of the Palacos® reaction is primarily dependent on the level of the intramedullary pressure in the shaft of the femur. The following measures are beneficial to prevent or reduce a Palacos® reaction:
Waiting for polymerization of the bone cement monomers before inserting into the shaft.
Using vacuum-operated mixers to minimize air bubbles within the PMMA cement.
Copious washing out of the bone shaft before insertion of the cement.
Airing/draining the shaft during the cementation.
Slow, focused insertion of the prosthesis into the femur shaft.
Balanced volume replacement and cardiovascular stability and prophylactic ventilation with 100 % oxygen are recommended.
11.1.6 How Will You Treat This Acute Situation?
The treatment is primarily symptomatic. Vasopressors and volume are administered to increase right ventricular filling. Sometimes, epinephrine or continuous infusions of another catecholamine are necessary. Increasing the inspiratory oxygen concentration to 100 %, or beginning assisted mask ventilation with 100 % oxygen during regional anesthesia, decreases the pulmonary arterial pressure and assures significant oxygenation.
>> CRNA Jennifer was now very nervous; the orthopedic surgeons could be heard hammering in the background. “What is wrong with the patient? Did she have a fat embolus?” she asked Dr. Pru. Jennifer reached the anesthesiologist-in-charge; he said he would come right away. She called other CRNAs to help, but they were busy with their patients at the moment. She questioned Dr. Pru further, “Should I do a blood gas analysis? Should I draw up more medications?” Dr. Pru declined the arterial blood gas as she had other problems to deal with at the moment.
11.1.7 Are You in Agreement with Dr. Pru’s Decision? What Further Information Would You Obtain? How Is Fat Embolism Diagnosed?
Actually, a blood gas would have yielded important diagnostic information in this situation. As discussed in Sect. 11.1.5, the patient could have suffered from a fat embolus. The diagnosis of fat embolus is usually a clinical diagnosis, with consideration of the possible causes. The classic triad consists of:
Respiratory insufficiency
Neurological changes
Petechiae on the upper extremities
Besides this, there are countless unspecific signs such as fever, tachycardia, renal failure, lab changes such as anemia, and coagulopathies. In serious cases, chest X-ray shows lung edema; the ECG may show signs of right heart strain. There are two theories for the pathogenesis of the so-called fat embolus syndrome.
11.1.7.1 Mechanical Theory
In the mechanical theory, it is assumed that large fatty drops cause blockage in the pulmonary arterial vessels and small drops may pass through the pulmonary circulation. This leads to microembolism in the central nervous system, the kidneys, and other organs, with the respective clinical signs and symptoms. The extrapulmonary signs could also be explained by a patent foramen ovale [1].
11.1.7.2 Biochemical Theory
The biochemical theory postulates the direct effects of the free fatty acids on the pneumocytes. Accordingly, hypoxia, hypertension, and the respective cardiopulmonary malfunction are explained.
A pulmonary embolus, besides increasing the pulmonary arterial pressure, also acutely increases dead space ventilation with an increase in the arterial alveolar CO2 difference. Therefore, it would be interesting to know:
The end-tidal CO2 concentration in comparison to the arterial CO2 concentration
The comparison of the current CVP with previous values
In the presented situation, Dr. Pru must decide if she can manage without the presence of CRNA Jennifer. She decided correctly, because carrying out an arterial blood gas analysis requires additional personnel resources. The end-tidal CO2 concentration and the CVP can be determined in the OR without additional effort.
>> The phenylephrine and the crystalloid infusion had no effect. Mrs. Moore’s systolic blood pressure had now dropped below 30 mmHg; her heart rate was only 30 beats/min. “We must start chest compressions immediately, or Mrs. Moore will die,” Dr. Pru announced loudly, so everyone could hear. The surgical team began immediate strong chest compressions. CRNA Jennifer prepared 1 mg epinephrine as soon as she heard the words “chest compressions.” After 30 s, and the split administration of 0.3 mg epinephrine, the blood pressure improved. The anesthesiologist-in-charge Dr. Eldridge walked in the door just as 0.3 μg/kg min of norepinephrine was being started as a continuous infusion to stabilize the blood pressure. He affirmed Dr. Pru’s decision. It took another 60 s before the S p O 2 had normalized.
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