RHABDOMYOLYSIS FOLLOWING CARDIAC SURGERY FOR ACUTE AORTIC DISSECTION

Introduction :Rhabdomyolysis is an uncommon complication during or after cardiopulmonary bypass ( CPB ). A correlation of rhabdomyolysis with femoral artery cannulation , prolonged duration of operation , low cardiac output and utilization of some drugs (isoflurane, enoximone, isoflurane and continuous intravenous infusion of epinephrine ) has been identified. We report a case of an adult patient with acute aortic dissection who developed severe postoperative rhabdomyolysis with acute renal failure requiring dialysis. Case report: A 23 Years old weight patient (weight ,110 kg;height 192 cm) complains of acute thoracic pain and had been computed tomography and transesophageal echocardiography diagnosed with acute aortic dissection , type II DeBakey aortic coarctation and pericardial effusion. He was urgently operated . The surgeon used removal of the ascending aorta and replacement with a synthetic graft Bard 25 under CPB. Family history was unremarkable and the patient had not been previously anesthetized. The patient was monitored using a radial arterial catheter, an internal jugular central venous catheter , rectal thermometer. Serial analyses of arterial blood gases and electrolytes were measured. Intraoperative transesophageal echocardiography was used to asses ventricular performance. Anesthesia was induced with dormicum 3 mg, pancuronium 8 mg , fentanyl 0.5 mg. After endotracheal intubation ,anesthesia was maintained with isoflurane, 0,8-to 1% ( end tidal concentration )and morphine 30 mg. Anesthesia under CPB was maintained with propofol 2-4 mg/kg/h. Eighty minutes after induction and before CPB ,the anesthesiologist observed an unusual hyperkalemia (K) of 7.33 mmol/L without hyperthermia . Figure 1 shows the evolution of hyperkalemia. The temperature before CPB was stable at 36.5 C , the temperature during CPB was in accordance with the surgical procedure replacement of the ascending aorta with a synthetic graft (cooling to 28C). At the end of CPB the temperature was 36C. The arterial site of cannulation were : the right femoral and the right subclavian arteries. During CPB , blood flow rate was between 1.7-2.4 ml/min/m2 with a stable mean arterial pressure at 60-80 mmHg. Blood gases were regulated according to stat regimen. The gas flow was doubled from the initial 1.6 L/min to 4.5 L/min , in an attempt to correct a hypercapnia (PaCO2, 57 mmHg ; pH=7.11 ). The PaCO2 decreased to 49 mmHg. Figure 2 shows the development of the temperature, pH and PaCO2. Transesophageal echocardiography showed good biventricular function and the patient was successfully weaned from CPB without any inotropes. During the rewarming phase a conventional ultra filtration was started . The target volume for ultrafiltrat removal was 4000 mL to achieve a zero fluid balance at the end of CPB and to correct hyperkalemia. The cross clamp time was 119 minutes and the CPB time 117 min.

After surgery , the patient was admitted to the intensive care unit. The first postoperatively 24 h was marked by: maximum rectal temperature was 37.7C ;the chest drainage 275 mL, PaCO2 between 40 and 42 mmHg and the patient was extubated . Vasodilator drugs ( nitroglycerin , diltiazem ) were used to maintain a deliberate systolic blood pressure below 100-110 mmHg ,in an effort to decrease blood loss. Diuresis after intermittent furosemide boluses was between 50 and 100 mL/h clear urine. On the day 1 ,the patient complained of pains in his right calf. The lab constants showed: serum creatinine Kinase ( CK )=11889 U/L , K=6.9 mEq/L , serum creatinine (CR) =3.3 mg/dl . Diuresis stimulated with furosemide is lower than 50 mL/h. A diagnosis of rhabdomyolysis and acute oliguric renal failure is made. Aggressive continuous veno-venous hemofiltration ( CVVH ) was used with ultra filtration rate at 3-4L/h under non-fractioned heparin 1000-1400 IU/h with ACT 155-200 s and serum levels AT III 53 %.Clotting of the circuit after 4 hours demanded it to be replaced and administration of 1000 IU of AT III. The constantly increasing K values of 6.1 to 6,3 mEq/L under CVVH lead to the option of continuous veno-venous hemodialysis with the following settings: blood flow=300ml/min ,dialysate flow =3000ml/h , removal rate=300-700 ml/h thus maintaining kalemia at values lower than 5 mEq /l. On postoperative day 3 , CK values over 13000 U/L and emergence of a compartment syndrome on the right calf required decompression fasciotomy. On the following days CK was noticed to be lower , down to 857 U/L on day 11. The serum myoglobin followed the same evolution ( FIG.4 ) decreasing from values over 700 ng/mL to 101 ng/mL. After two procedures of CVVHD and four of CVVH ,on day 6 , diuresis goes beyond 150 mL/h. CR decrease slowly reaching 1.2 mg/dL on day 33. Fig. 3 shows the evolution of renal function. On day 21 a reoperation is performed to remove a pericardial effusion under general anesthesia using propofol , ketamine and atracurium. By means of subxiphoidian drainage 800 mL serohemorrhagic liquid was extracted. The patient is released from the intensive care unit after 28 days . He was discharge in good condition rhabdomyolysis the thirty-third postoperative day . Discussion Rhabdomyolysis is the lyses of muscle tissue from a traumatic ,toxic or metabolic insult. In this case the cause of rhabdomyolysis could include: 1)interruption of the vascular supply of a limb by femoral artery cannulation (ischemia followed by reperfusion after decannulation. 2)drug induced rhabdomyolysis ( isoflurane,protamine) occurs via electrolyte imbalance or induction of malignant hyperthermia. Early systemic hyperkalemia ( K> 7.33mmol/L ) was the first sign of rhabdomyolysis The Diagnosis is made in the presence of an elevated CK and clinical history. Rhabdomyolysis may or may not result in visible myoglobinuria since the achievement of myoglobinuria depends on the amount of myoglobin released from the muscle , the plasma concentration of myoglobin and glomerular filtration rate and urine flow rate. Diagnosis was missed, in the first 24 h, when clinical symptoms are minimal and urine was clear. A five fold increase in the serum creatinine kinase (> 1000 IU/L) without cardiac and brain injury is the single most sensitive diagnostic criteria for rhabdomyolysis. A ten or more fold increase in the Ck was noted for rhabdomyolysis after cardiac surgery ,as in our case (CK>13000). CK elevation appears proportional to the quantity of muscle injured.

Ck levels decline by about 40% per day and a constant level suggest ongoing muscle damage , for this patient with a developing muscle damage, demanding fasciotomy. Acute renal failure (ARF ) The severity of the ARF is proportional to the amount of crushed muscle ,but the rhabdomyolysis is not the only cause of ARF. The development of renal failure could be explained by: 1)Extracorporeal circulation is associated with multiple perturbation in renal physiology and function. During CPB the renal blood flow and glomerular filtration rate decrease with 25-75 % and renal vascular resistance increases. 2) Aortic dissection with pericardial effusion and aortic coarctation is at high risk for postoperative ARF by the secondary hypotension and hypo perfusion. 3)Myoglobin ( Mb ) is directly tubulotoxic via free radical mediated injury. Mb precipitates in the tubules causing tubular obstruction , involved in the genesis of the ARF Some modes of renal replacement therapy may be able to reduce the Mb burden on the kidney. Considerable amounts of Mb can be removed by high ultra filtration rate CVVH. But once ARF developed the method of blood purification should be selected for its effectiveness in treating ARF and its manifestation rather than elimination of Mb. Sustained hyperkalemia ( caused by ongoing muscle damage in the presence of ARF) despite the use of aggressive CVVH required to change it to CVVHD. Severe hypercapnia ,muscle rigidity , hyperthermia and rhabdomyolysis characterize malignant hyperthermia ( MH ) in fulminate form. Possibility of MH in a sub clinical form ( hypercapnia during CPB and rhabdomyolysis in the ICU ) Should be considered ,in this patient who received isoflurane . In a second step this patient needs to be investigated for MH susceptibility. During cardiac operations using CPB the diagnosis may be obscured by the temperature changes during CPB and by the convective middle molecules ( MB ) clearances on conventional ultra filtration. Conclusion 1) Rhabdomyolysis is a complication of cardiac surgery under CPB. 2) The early systemic hyperkalemia was the first sign of rhabdomyolysis ( and MH ). 3) CVVHD is an effective technique to rescue acute myoglobinuric renal failure. 4) The peculiarities of the case are: the association of acute aortic dissection with aortic coarctation ; early onset of rhabdomyolysis before CPB ; development of acute oliguric renal failure requiring renal replacement therapies