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Thoraco-abdominal Aneurysm : Anaesthetic Challenge
Rochana G Bakhshi*, Lalita V Dewoolkar**
Thoraco abdominal aneurysms are frequently treated without the use of cardiopulmonary bypass. Anaesthetic management of these patients is extremely challenging because of the significant haemodynamic changes associated with the operation, patient positioning, one lung ventilation and frequent co-existing cardiovascular disease as well the risk of spinalcord, renal and mesenteric ischaemic injuries. Anaesthesiologist must be prepared for rapid and massive blood loss and coagulopathy. Since repair is frequently performed without the use of cardiopulmonary bypass, one must rely on peripheral sites for rapid fluid resuscitation. Simple clamp and sew technique without the use of temporary shunts or partial bypass techniques usually requires significant pharmacologic interventions in order to treat proximal arterial hypertension and to protect the myocardium. Nitroglycerin is helpful in reducing preload and cardiac filling pressure. It can be used in combination with nitroprusside and/or isoflurane (low to moderate concentrations). Prior to unclamping vasodilators need to be discontinued and vasopressors should take their place i.e. before release of the clamp.

A true aortic aneurysm is a dilation of aorta as measured across from one endothelial wall to the other. The wall consists of attenuated layers of the normal aortic wall, unlike a false aneurysm, which has a normal internal diameter with bulk of the aneurysm originating from a dissected channel, the wall of which consists of aortic adventitia and compressed periaortic fibrous tissues.

Atherosclerosis accounts for approximately 95% of abdominal aneurysms, only 50% of thoracic and thoracoabdominal aortic aneurysms belong to this category.1 The remainder are caused either by trauma or by conditions such as Marfan syndrome, cystic medial degeneration, Takayasu arteritis or syphilitic aortitis.

Thoracoabdominal aneurysms were classified by Crawford into four types:

Type I : Includes most of the descending thoracic aorta and upper abdominal aorta (suprarenal).

Type II : Most of the descending thoracic aorta and most of abdominal aorta.

Type III : Lower portion of the descending thoracic aorta and most of abdominal aorta (including renal and visceral arteries).

Type IV : Most or all of the abdominal aorta.

Case Report

Sixty one year old married housewife was brought in emergency hours with the chief complaints of : Haemoptysis 5 days ago, small amounts not associated with haemodynamic instability or altered sensorium.

Pain in upper abdomen, mainly epigastrium, dull aching type, radiating to the back and not related to meals. Recurrent episodes of fever off and on, moderate to low grade since 1 month, treated by private doctor.

She was a known diabetic since 6 years, was on oral hypoglycaemic agents, but since 1 month, on actrapid insulin 8-8-8-0 and insulatard 0-0-0-8 units.

She was suffering from hypertension since last 6 years and was on Tab. Amlodipine 5mg OD for the same.

She had undergone right knee surgery for pyoarthrosis 3 years back and debridement for carbuncle on the back 2 months back. No history of koch's or koch’s contact, epilepsy, bronchial asthma, palpitations etc.

On examination, her general condition was fair, pulse rate : 98/min, regular blood pressure : 130/80 mmHg in right brachial supine position.

Respiratory rate : 16/min, jugular venous pressure not raised, respiratory system on auscultation, had bilateral rhonchi. Heart sounds were normal, per abdomen, she had ill defined tenderness in the epigastric region.

Abdominal ultrasonography showed 4.1 cm x 4.9 cm x 5.3 cm saccular aneurysm of the descending aorta, 3 cm superior to the coeliac trunk.

C. T angiography: saccular aneurysm of the descending thoracic aorta and upper abdominal aorta extending from the carina upto the origin of coeliac axis. Neck of the aneurysm approximarely 1cm in diameter at the level of gastro-oesophageal junction. A large thrombosed component measuring approximately 3 cm seen within the aneurysm. Descending thoracic aorta was displaced to the left with the aneurysm placed medially. A 1 cm nodule in right upper lobe of lung with central cavitation of tuberculous aetiology.

Patient was subjected to coronary angiography which was normal. ECG was normal, X-ray chest PA view showed left ventricular hypertrophy.

Blood investigations :


Preoperatively, two 16 gauge peripheral lines were established. The internal, jugular vein was cannulated using a triple lumen catheter. Intraarterial cannulae were inserted in right radial and right femoral arteries for continuous pressure monitoring. One lumen of the triple lumen catheter was used for central venous pressure monitoring.

Patient was induced with thiopentone sodium 5mg/kg and succinylcholine 2 mg/kg sedation given was inj. Midazolam 1.5 mg i.v. Analgesia was achieved with Buprenorphine 90 mgm. Patient was intubated with 7.5 portex cuffed endotracheal tube, it was inserted on the right side in order to achieve preferential right sided ventilation and thereby trying to maintain one lung ventilation during the procedure.

Relaxant used was pancuronium 0.1 mg/kg. Lower tidal volume and higher respiratory rate was used during procedure. Patient was in right lateral position. The aneurysm was exposed via left thoracoabdominal incision.

Aortic cross clamp time was 30 minutes. Prior to clamp application, patient was given mannitol 20%, 0.25 gm/kg. Dopamine 3 mcg/kg/m was started. Inj. Methyl prednisolone 1gm i.v. was given. One pint of blood was started slowly and other two lines had crystalloid infusion (Ringer lactate). After clamp application, initially blood pressure rose to 160/90 mmHg and then gradually within next 10 minutes dropped upto 120/70 mmHg, but was maintained at that level. NTG infusion was therefore not started for this patient. Repair was done in 30 mins. Just prior to release of clamp, 3 pints of blood, followed by 3 pints of fresh frozen plasma were given and thereafter total of 7 pints of blood and fresh frozen plasma were given. After release, blood pressure dropped upto 80 mmHg, thereafter was maintained at 90-100 mmHg systolic. Urine output during clamp period was 170 ml. Dopamine was increased to 7 mcg/kg/min, lung ventilation was established by withdrawing the tube slightly. Acidosis during the procedure was corrected using sodabicarb as an infusion. Tidal volume was increased. Haemostasis was achieved by surgeons and then closure started. Patient was shifted to ICU prophylactically on ventilator and was extubated next morning.


Aortic aneurysms usually occur in the sixth to seventh decade of life. It affects men more than women. Incidence of COPD in patients with thoracoabdominal aortic aneurysms ranges from 30% to 50%. Patients may also have associated coronary, renal and cerbrovascular arterial atherosclerosis. 50% of patients with abdominal aortic aneurysms and 70% of patients with thoracoabdominal aortic aneurysms are hypertensive.2

Preoperative evaluation of renal and cardiac function is very important to predict post operative outcome.

Preoperatively atleast 15 units of packed red blood cells and 15 units of thawed fresh frozen plasma should be immediately available and additional units should be obtainable. Saleh has recommended four 14G peripheral intravenous catheters, two in the upper extremities and two in the lower extremities to rapidly replace volume. Blood warmers and rapid infusion sets should be available. We also cannulated right internal jugular vein using a triple lumen catheter. All patients undergoing aortic surgery should have continuous intra arterial monitoring of blood pressure. In addition to radial pressure monitoring, femoral arterial cannula is recommended in patients undergoing thoracic or thoraco abdominal aneurysm surgery which will permit monitoring of distal aortic perfusion pressure and adjustment of bypass flow as necessary to maintain adequate spinal cord and visceral perfusion. Our patient already had a right femoral cannula in place, she had undergone emergency coronary angiography on the same day, which was normal. Patients should receive their preoperative usual doses of medications such as beta blockers, calcium channel blockers and anti hypertensive agents. Proper premedication and sedation in form of opiods by intramuscular route and oral benzodiazepines may be administered to prevent anxiety, tachycardia and hypertension. Prophylactic antibiotics administered preoperatively result in a lower rate of post operative infection in patients undergoing vascular surgery. Proper hydration before resection of aneurysm helps prevent the extreme changes in blood pressure during surgery.2

Induction of anaesthesia should be slow and controlled without hypertension because stress on the aneurysm can cause rupture. Heart rate should be maintained near baseline because myocardial ischaemia is often rate related. Balanced anaesthetic technique for aneurysm induction usually involves a combination of an opiod, a low dose potent inhalation agent, a benzodiazepine and a long acting muscle relaxant.

Descending thoracic aneurysms are best approached through a left thoracotomy incision, with patient in right lateral decubitus position. One lung ventilation using a double lumen tube (DLT) is extremely helpful as, by collapsing the left lung surgical exposure is better. If aorta is adherent to related structure, it would require delicate dissection and mobilization. Use of this technique would also protect the dependent lung from any spill over of blood that results from surgical manipulation and retraction of nondependent part.3 Placement of left sided DLT can be difficult because of anatomic displacement of the left main bronchus by the aneurysm. Our attempts to pass a DLT were unsuccessful probably due to compression of the left bronchus by the aneurysm, which led to malpositioning. Other options are use of a right sided endobronchial tube or single lumen endotracheal tube and left bronchial blocker. We passed a single lumen endotracheal portex tube and inserted it on the right side. Inspired oxygen concentration of 1.0 should be used during one lung ventilation to protect against hypoxaemia.3 Collapse of the non ventilated, non-dependent lung results in hypoxic pulmonary vasoconstriction (HPV). This causes local increases in pulmonary vascular resistance (PVR) and diversion of blood flow to the other better oxygenated lung. Standard monitoring should include pulse oximetry, capnography, body temperature and electrocardiography. Foley’s catheter for urinary output is a must. Lead II is extremely helpful in diagnosing dysrhythmias and V-5 lead in detection of myocardial ischaemia. Continuous intra arterial monitoring of blood pressure should be done. Intra -operatively we also did serial arterial blood gas analyses and accordingly were correcting the acidosis with sodabicarb. Pulmonary artery catheter may be placed for measuring cardiac filling pressures and cardiac output. Spinal cord function monitoring is done using somato sensory evoked potentials, motor evoked potentials and cerebrospinal fluid pressure monitoring.

Simple aortic cross clamping consists of clamping the descending thoracic aorta proximal and distal to the aneurysm without the use of shunt or pump. This is the simplest method for resection in the shortest period of time. Disadvantage of this technique are distal organ ischaemia, proximal arterial hypertension and metabolic acidosis. A cross clamp time exceeding 30 minutes is associated with the risk of spinal cord injury. Clamping of the aorta causes hypertension in the proximal segment and hypotension in the distal segment. Mean arterial pressure usually increases by approximately 40% after cross clamping the descending thoracic aorta. Arterial pressure below the cross clamp decreases to approximately 15% of the values before cross-clamping, with distal aortic pressures ranging between 11 and 30 mmHg.4 Central venous pressure usually increases slightly by approximately 2-4 mmHg probably due to auto transfusion of blood from the lower extremities. In a fully developed collateral flow, aortic clamping may result in no pressure change proximal or distal to the clamp. Cross clamping of descending thoracic aorta results in lowered total body oxidative metabolism and oxygen consumption as well as conversion to anaerobic metabolism by the ischaemic body mass distal to the clamp. Cross clamping of the descending thoracic aorta without the use of shunt produces hypoperfusion and anaerobic metabolism in the splanchnic viscera and lower extremity. Lactate concentration promptly rises during clamp period. A continuous infusion of sodium bicarbonate at the rate of 0.05 meq/kg/min is recommended throughout the period of clamp. Bolus administration immediately after unclamping may further increase PaCo2 and worsening of intracellular acidosis.5 With clamp application, vasodilation therapy may be started as required. During this period, intravascular volume should be maintained and replenished, using crystalloids, colloids, and if necessary blood transfusion. Aggressive fluid replacement should be done for the insensible surgical losses due to exposure of abdominal contents. Prior to unclamping vasodilator infusions should be discontinued, ventilation should be increased in anticipation of an increased acid load from the distal circulation. Dopamine infusion should be available to treat hypotension.

Renal protection and prevention of spinal cord ischaemia is of prime importance during aneurysm surgery. Clamping of the aorta for more than 1 hour carries high risk of acute renal failure. Thoracoabdominal aneurysm surgeries in which renal arteries and kidneys are exposed, the kidney can be perfused with cold crystalloid solution or subjected to surface cooling. Pharmacologic renal protection includes use of diuretic drugs such as mannitol or furosemide. Dopamine in the dose of 1-3 mcg/kg/min dilates renal blood vessels and improves renal blood flow and diuresis. Pretreatment with calcium channel blockers has been found to limit degree of ischaemic renal injury.

Other than the location and extent of aneurysm, the duration of cross clamp on the aorta is the single most important determinant of paraplegia and renal failure when bypass is not employed. Clamp times of less than 20-30 minutes are associated with almost no paraplegia. More than 30 minutes, there are higher chances of paraplegia. Pharmacologic protection may be achieved with corticosteroids, mainly Methylprednisolone. Calcium channel blockers also reduce calcium influx following ischaemic and reperfusion injury. Oxygen free radical scavengers such as superoxide dismutase also exert a protective effect by counteracting effects of oxygen free radicals produced during the ischaemic interval. Pharmacologic antagonism of NMDA receptor neurotoxicity may provide a new approach in attenuating the effects of spinal cord ischaemia.

Dean and Dr. LS Chaudhari Head Department of Anaesthesiology, Seth GS Medical College and KEM Hospital, Mumbai 400012.
1. Culliford AT, Ayvaliotis B, Shemin R, Colvin SB, Isom OW, Spencer FC. Aneurysms of the descending aorta. J Thorac Cardiovasc Surg 1983; 85 : 98.
2. Banoub M, Kagan-koepke TD, Shenaq S. Anaesthesia for thoracic aortic surgery In: Estafanous FG, ed. Cardiac anesthesia:principles and clinical practice. Philadelphia: JB Lippincott, 1994; 553 : 559.
3. Benumof JL. Physiology of the open chest and one-lung ventilation. In: Kaplan JA, ed. Thoracic anesthesia. NewYork : Churchhill Livingstone, 1983; 278.
4. Silverstein PR, Caldera DL, Cullen DJ, et al. Avoiding the hemodynamic consequences of aortic cross clamping and unclamping. Anesthesiology 1979; 50 : 462.
5. Saleh SA, Crawford ES, Bamberger RA. Intraoperative acid base management for the resection of thoraco abdominal aneurysms: A comparison of continuous infusionof Sodiumbicarbonate versus bolus. Anesth Analg 1982; 61 : 213 (abstract).