ANESTHETIC MANAGEMENT OF PRE-INDUCTION SUBACUTE …

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Int. J. Pharm. Med. & Bio. Sc. 2014 Soniya R Sulhyan et al., 2014

ANESTHETIC MANAGEMENT OF PRE-INDUCTION

SUBACUTE LEFT VENTRICULAR WALL RUPTURE:

A CASE REPORT

Soniya R Sulhyan1*, Anand T Vagarali1, Sharangouda S Patil1 and Mahadev D Dixit1

Case Report

Rupture of the free wall of the Left Ventricle (LV) is a fatal complication of acute myocardialinfarction (AMI). The clinical presentation varies from the acute form which has a high mortalityrate to the formation of a pseudoaneurysm. Sudden electromechanical dissociation in theOperating Room (OR) has many clinical possibilities and it warrants rapidious surgical interventionin a hemodynamically unstable patient. This rare case report discusses the challenges facedby the anaesthetist in the diagnosis and management of a subacute form of left ventricular freewall rupture (LVFWR) before the induction of anaesthesia in the OR.

Keywords: Subacute left ventricular wall rupture, Anesthetic management, Acute myocardialinfarction, Electromechanical dissociation

*Corresponding Author: Soniya R Sulhyan � [email protected]

INTRODUCTION

Left ventricular free wall rupture (LVFWR) is a

fatal, infrequent and serious complication of acute

myocardial infarction (AMI) occurring in 2-4% of

patients (Palwasha Sahibzada et al., 2009). It is

the second most common cause of death after

AMI (James Figueras et al., 1997) and accounts

for approximately 20% of infarct related deaths

(Luis Raposo et al., 2006). Rupture generally

occurs between 1-7 days after the AMI (Nicholas

T Kouchoukos et al., 2013). An acute LV wall

rupture leads to sudden extravasation of blood

from the ventricle into the pericardial cavity,

causing acute cardiac tamponade. This event

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Int. J. Pharm. Med. & Bio. Sc. 2014

1 Department of Cardiothoracic and Vascular Anesthesia and Surgery, KLE University’s Jawaharlal Nehru Medical College, Krishna floor, Near

ITU (Intensive Therapy Unit), Dr. Prabhakar Kore’s Hospital and Medical Research Centre, Nehrunagar, Belgaum-590010, Karnataka, India.

leads to decrease in the circulating blood volume

in the body producing signs and symptoms of

shock. It also significantly compromises the

diastolic filling of the left ventricle due to LV

compression by the enormous amount of blood

in pericardial cavity thereby decreasing the

perfusion to all organs. The present rare case

report is of subacute LVFWR leading to

electromechanical dissociation occuring just

before induction of anesthesia.

CASE PRESENTATION

A female patient aged 76 years, who had recent

anterior wall myocardial infarction (AWMI) and

was thrombolysed with Inj. Streptokinase, was

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admitted to the hospital for ongoing chest pain

and shortness of breath. She was a known

hypertensive and was euthyroid and therefore

was not on thyroid supplement for hypothyroidism.

She underwent coronary angiography which

revealed critical Left Main (LM) artery stenosis

with thrombus in the LM extending to proximal

left anterior descending artery (LAD) and proximal

left circumflex artery (LCX). In addition, she had

plaque in mid LAD. Her right coronary artery

(RCA) was normal. Her transthoracic

echocardiography (TTE) revealed LV dysfunction

with ejection fraction (EF) of 40%. Her distal

Interventricular Septum (IVS), apex, and anterior

wall were a kinetic. Mild pericardial effusion was

present.

Because of her ongoing chest pain, she was

taken up for emergency coronary artery bypass

grafting (CABG). After shifting her to OR and while

the electrocardiography (ECG) electrodes were

being applied, she had sudden cardiac arrest.

She was immediately intubated with 8 mm portex

cuffed endotracheal tube under vision without any

inducing drugs or muscle relaxants. A peripheral

venous cannula of 16 G was inserted immediately

and Inj. Adrenaline given IV. Emergency

sternotomy was done, only to find the pericardium

full of fresh blood and clots, which had lead to

cardiac tamponade. A rent was seen in the

infarcted anterior region of LV. Emergency

cardiopulmonary bypass (CPB) was set up with

right atrial cannulation with arterial cannulation to

ascending aorta after adequate heparinization.

Patient was cooled to 28oC. The rent in the LV,

i.e., the ruptured akinetic portion of LV was excised

and surgical restoration of LV was done using

polytetrafluroethylene (PTFE) felt on either side

of ruptured LV edges and double layer

approximation of PTFE felt and refashioned LV

edges using 1 no. Ethicon 30 mm needle (Figure

1). CABG x 3 grafts were done, anastomosing

Saphenous Vein Grafts (SVG) to LAD, Obtuse

Marginal 2 (OM2) and Posterior Descending (PD)

arteries. A 7.5 Fr 16 cm triple lumen central venous

catheter was inserted into the right subclavian vein.

Patient was then rewarmed and successfully

weaned off with inotropic support and intraaortic

balloon pump (IABP) support. However, chest wall

closure was deferred and patient shifted to ITU.

Figure 1: Intraoperative Photograph of LVFree Wall Showing the Extensive RupturedPortion Secured with PTFE Felt on EitherSide of Ruptured LV Edges and DoubleLayer Approximation of PTFE Felt and

Refashioned LV Edges Using 1No. Ethicon 30 mm Needle

On 2nd postoperative day, the chest was

closed. Patient continued to do well and on 5th

postoperative day her IABP was removed.

Her renal parameters were deranged in the

postoperative period. She had to be reintubated

and her renal failure progressed and she went

into low cardiac output. Hemodialysis was not

possible because of hypotension. She had

cardiac arrest on 8th postoperative day and inspite

of all resusciative measures, she died.

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DISCUSSION

The time of occurrence classifies post AMI

LVFWR into two subtypes, early and late;

occurring 48 hours before and after the episode

of acute MI (Figueras et al., 2000).

There are 3 forms of post- AMI LVFWR

classified according to the time of occurrence and

form of presentation. The acute form of ventricular

rupture is the most common form usually

occuring on the first day of AMI and is fatal. Acute

LVFWR leads to acute cardiac tamponade due

to rapid development of massive hemopericardium

and compromises diastolic filling of both left and

right ventricles leading to decreased stroke

volume and cardiac output. This leads to rapid

electromechanical dissociation and sudden

death. The “oozing type” or subacute form is

marked by small leak through a friable myocardial

tissue leading to pericardial effusion without

significant cardiac tamponade. As in our case,

acute blowout rupture can occur in the subacute

form after initial AMI if left untreated (Figueras et

al., 2000; Qiping Chenet al., 2004; and James W

Bard, 2000). The third type is the “chronic type”

which leads to the pseudoanerysm formation

(Qiping Chen et al., 2004; and James W Bard,

2000).

LV ruptures are also classified into 4 patterns.

Type I has an almost direct trajectory with little

dissection. Type II has a multicanalicular trajectory

with extensive myocardial dissection and bloody

infiltration. Type III has the orifice of rupture

protected either by a thrombus or by a pericardial

symphysis. Type IV is an incomplete rupture such

that the trajectory does not extend completely

through the muscle (Hasan Ekim et al., 2009).

Risk factors for ventricular free wall rupture

after an acute MI include female gender, older age,

hypertension, single vessel disease, and

transmural infarctions with relatively good

ventricular function and AWMI (Qiping Chenet al.,

2004; and Hasan Ekim et al., 2009).

Sudden hypotension and bradycardia with

cyanosis and loss of consciousness is an

indicator of impending rupture (Hasan Ekim et

al., 2009). LVFWR should be suspected in

patients who have recurrent or persistent chest

pain after an acute transmural infarction,

hemodynamic instability, syncope, signs of

pericardial tamponade-neck vein distension,

cyanosis, pallor, shock with hypotension, pulsus

paradoxus, elevated venous pressure, quiet heart

sounds, diastolic equalization of central venous

pressure (CVP), pulmaonary artery pressure and

pulmonary capillary wedge pressure, steep X

descent and blunted Y descent on CVP, sinus

bradycardia, nodal rhythm or transient

electromechanical dissociation (Nicholas T

Kouchoukos et al., 2013; Figueras et al., 2000;

James W Bard, 2000; and Hasan Ekim et al.,

2009).

ECG shows low voltage QRS complex,

electrical alterans, T wave changes.

Echocardiogram shows pericardial effusion with

or without evidence of cardiac tamponade.

Pericardiocentesis may be useful for establishing

the diagnosis of hemopericardium and therapeutic

for relieving the tamponade (James W Bard,

2000).

Successful medical management of subacute

LVFWR has been reported. Percutaneous

intrapericardial fibrin-glue injection therapy (PIFIT)

has been tried as an alternative for LVFWR

instead of surgical repair and has found to be quite

effective (Masayoshi Terashim et al., 2008).

Extracorporeal Membrane Oxygenation (ECMO)

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can also be used as a bridge to recovery or for

safer surgery after 7 to 10 days (Golbarg Abedi-

Valugerdi et al., 2012). But surgical therapy

appears to be the definite therapy (Figueras et

al., 2000; and James W Bard, 2000). Surgical

repair can be achieved by 3 surgical techniques.

Direct closure with suture reinforced by Teflon

felt is used for small lacerations. Infarctectomy

and Teflon felt–reinforced suture closure is

possible in small infarctions. A rent can be closed

with a felt sandwich, bovine pericardium or

prosthetic patch using various novel techniques

like double patch sealing method secured by

glues, sutures or both (James W Bard, 2000; and

Hideki Amano et al., 2002). Sutureless techniques

have also been used, for example in slow

leakages (Golbarg Abedi-Valugerdi et al., 2012).

PTFE felt, polyester or pericardial patches can

be placed over the site of rupture and sutured

with various glues like Gelatin-Resorcin-

Formaldehyde-Glutaraldehyde (GRF), fibrin,

cyanoacrylate (Nicholas T Kouchoukoset al.,

2013).

This is a case of subacute LVFWR which

progressed to acute blow out rupture. There are

two possibilities, either it is a case of acute on

subacute rupture, and not a case of acute rupture

because it occurred on the 9th day after AWMI

because Kirklin et al. say that acute rupture

usually occurs between 1- 7 days of acute MI

(Nicholas T Kouchoukoset al., 2013), or it is a

delayed form of acute rupture. Diagnosis of acute

on subacute rupture of the LV free wall is difficult

in the OR, mainly because of the differential

diagnoses like acute massive pulmonary

embolism, acute anaphalactoid reaction to

antibiotics because these are usually given before

induction and spontaneous tension pneumothorax

because of ruptured emphysematous bullae

(Qiping Chen et al., 2004). The diagnosis of

subacute LVFWR is mostly made from diagnosis

of hemopericardium and cardiac tamponade by

two dimensional echocardiography (James Slater

et al., 2000), cardiac catheterisation or

pericardiocentesis and the signs associated

thereof (Augusto Purcaro et al., 1997). To the

authors’ best knowledge, there are no reported

cases of spontaneous subacute LVFWR on the

operating table in the OR just before induction of

anaesthesia. Such a condition, provides even no

time for placement of intravenous and intra-arterial

lines. Immediate institution of CPR with rapidious

placement of intravenous line for IV bolus of

resuscitation drugs is the key.

Role of IABP is very well established in

ventricular septal rupture secondary to AMI. But

its role in LVFWR is controversial (Nicholas T

Kouchoukos et al., 2013; James W Bard, 2000;

and Hasan Ekim et al., 2009). Placement of an

IABP by one part of the surgical team provides

afterload reduction and may buy time before

insertion of arterial and venous cannulae before

going on CPB. In this case, IABP was inserted

for optimizing coronary perfusion while

simultaneous sternotomy and manual direct

cardiac compressions were given.

Rapid infusion of blood and blood products is

very crucial in such case. On the cardiopulmonary

bypass, 3 packed cell volume units and 2 whole

blood units were added.

The post bypass anesthetic management is

very crucial in this case. Optimal hemodynamics

with mean arterial pressures to maintain adequate

perfusion pressures but to avoid excess strain

on the sutured LV wall is extremely important. The

spherical shape of the LV cavity changes from

spherical. Also, the LV volume is reduced. It also

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requires the use of inotropes to support the

contractility of the heart but to maintain the same

perfusion pressures and a urine output of 1 mL/

kg/h. In our case, high dosage of inotrope infusion

was required to maintain adequate pressures, IV

Dobutamine 10 mcg/ kg/ min, IV Adrenaline 0.15

mcg/kg/min and IV Vasopressin 1 U/hr. IV

Milrinone 0.5 mg/kg/min was also started later in

the postoperative period while decreasing the

Dobutamine dose. Fluid overloading must be

avoided.

Achieving optimal hemostasis in this case is

a challenge. The patient was on IV Heparin since

9 days. CPB also is a known cause for platelet

dysfunction and a trigger for initiation of a complex

cascade of coagulation, firinolysis and

inflammatory pathways. Heparin infusion was

needed to maintain ACT between 130-160 s due

to the presence of IABP. Chest closure was

deferred in our case because of unstable

hemodynamics.

Because of the rapid sterile cleaning and

draping of the patient, followed by deferred chest

closure postoperatively, IV Meropenem 1 g thrice

a day (TID) was started. IV Metronidazole 500

mg TID was started for covering anaerobic

infection.

Immediate recognition of subacute LVFWR is

a challenge and requires high degree of suspicion.

The immediate institution of CPR with immediate

insertion of IABP with emergency sternotomy,

followed by manual cardiac compressions and

rapidious institution of CPB with maintenance of

adequate perfusion pressures is a must. All these

measures were done to increase the perfusion

pressures. Since the patient hemodynamically

collapsed before placing any intravenous or

intraarterial catheters, recognition of arterial

pressures was not possible. Placement of

intravenous and one intraarterial catheter,

preferably radial should be encouraged

preoperatively in the preoperative room. There

was no evidence of cardiac tamponade or

pericardial effusion on the preoperative chest

radiograph. However, the TTE had revealed mild

pericardial effusion.

REFERENCES

1. Augusto Purcaro, Carlo Constantini, Nino

Ciarrpani et al. (1997), “Diagnostic criteria

and management of subacute ventricular

free wall rupture complicating acute

myocardial infarction”, American Journal of

Cardiology, Vol. 80, No. 4, pp. 397-405.

2. Golbarg Abedi-Valugerdi, Anders Gabrielsen,

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left ventricular rupture after myocardial

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3. Hasan Ekim, Mustafa Tuncer and Halil Basel

(2002), “Repair of ventricular free wall

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