Obstetric hemorrhage in a case of hypertrophic obstructive cardiomyopathy with automatic implantable cardioverter defibrillator: Anaesthesia and intensive care management.

The physiological changes occurring during pregnancy and labor may reveal or exacerbate the symptoms of hypertrophic obstructive cardiomyopathy (HOCM). The addition of obstetric hemorrhage to this presents a unique challenge to the anesthesiologists and intensivists managing these patients in the operation theatres and the Intensive Care Units. Here we present a case of HOCM with automatic implantable cardioverter defibrillator in situ and postpartum hemorrhagic shock.

INTRODUCTION

Hypertrophic obstructive cardiomyopathy (HOCM) is an uncommon form of cardiomyopathy that affects the interventricular septum in the area of the left ventricular outflow tract (LVOT), characterized by left ventricular (LV) hypertrophy, decreased LV chamber size, and LV dysfunction.[123] The physiological changes occurring during the pregnancy and labor may reveal or exacerbate the symptoms of HOCM.[34] Management of this condition involves medical, electrophysiological, percutaneous transluminal septal myocardial ablation, and surgical therapy.[5] Women of child-bearing age who are symptomatic or have a history of syncope are candidates for insertion of a pacemaker or an automatic implantable cardioverter defibrillator (AICD) before conception.[67] Below we are reporting an anesthetic and intensive care management of a case HOCM with the AICD devices in situ and postpartum hemorrhage (PPH).

CASE REPORT

A 23-year-old female was admitted with 9 months amenorrhea for safe confinement. She was a known case of HOCM with a permanent dual chamber pacer in situ for about 5 years and was on tablet diltiazem 30 mg thrice daily. She delivered a live full-term baby following which she had PPH. Episiotomy and low forceps were used during delivery. Repeated doses of uterotonics (oxytocin, carboprost) were tried. Tamponade also did not work and in view of deteriorating hemodynamics despite adequate intravenous (I.V.) fluid she was rushed to the operation theatre for definitive management. She had lost nearly one liter of blood in the labor room as assessed by the obstetrician.

She was taken up for emergency laparotomy to control PPH. She was drowsy, tachypnoeic, tachycardic and severely pale with SpO2 of 95% and systolic blood pressure (BP) <60 mm Hg. She had two 16 gauge I.V. cannulae in place. 500 ml of tetrastarch was rushed in, and BP improved to 80/50 mm of Hg. She was preoxygenated, and saturation improved to 100%. The patient was induced with titrated doses of I.V. fentanyl up to 70 µg, I.V. ketamine 30 mg and suxamethonium 75 mg. She was intubated and maintained with I.V. fentanyl along with nitrous oxide and oxygen and I.V. atracurium. Intraoperatively, left sided internal jugular vein (IJV) was cannulated with a 5 cm long 16 gauge I.V. cannula for resuscitation, the left side was preferred over the right because there was possibility of the guide wire of the central line getting entangled in the pacer wires or thrombus/clot around the pace wires. Left radial artery was cannulated, and invasive BP (IBP) was 86/52 mm Hg. Initially, internal iliac artery ligation was done, but as bleeding continued, the obstetrician decided to opt for a hysterectomy. Blood loss was 1.5 L, which was replaced with crystalloids, one colloid, and three units of packed cells. Central venous pressure (CVP) was 10–12 cm H2O. Intraoperatively saturation was 100% and mean arterial pressure was maintained at above 50 mm Hg.

The patient was shifted to the Intensive Care Unit (ICU) and connected to ventilator and monitors. IBP was 80/52 mm of Hg. After transfusion of another two packed red cells and 4 units of fresh frozen plasma, IBP started improving. She was extubated the next day, and her further course in the hospital was uneventful.

DISCUSSION

HOCM is characterized by hypertrophy of the cardiac musculature.[8] Asymmetric septal hypertrophy and LV hypertrophy leads to LVOT obstruction with a hypercontractile and poor compliant of left ventricle. Impairment of diastolic filling results in elevated LV end-diastolic left atrial and pulmonary pressures.[9101112]

The symptoms of HOCM include Dyspnea, chest pain, palpitations, dizziness, fainting, and sudden cardiac death.[10] Medical and surgical interventions include Beta blockade, calcium channel blockade, diuretics, septal myomectomy or ablation, or dual chamber pacing.[1013]

Perioperative management of these patients aims at maintaining the adequate preload and afterload. Avoiding vasodilators and agents that increase contractility are pivotal in the management of these patients. Intra-operative goals include maintaining sinus rhythm, minimizing stressful stimuli and minimizing or preventing dynamic LVOT obstruction.

Common causes of PPH are uterine atony, retained products of conception or coagulopathy. Risk factors include prolonged labor, multiple pregnancies, polyhydramnios, large baby, and previous uterine surgery. In this case, PPH was resultant of uterine atony. The options for management of such patients include: Resuscitation, uterotonics, uterine tamponade, instituting B-lynch suture, ligation of uterine and internal iliac arteries, compression/clamping aorta, radiological arterial embolisation or balloon occlusion or in resistant, torrential PPH, as in our case, hysterectomy. Tranexamic acid and recombinant factor VIIa also help in controlling bleeding.

The commonly used drugs for induction of anesthesia are thiopentone, ketamine, and propofol. Both thiopentone and propofol cause hypotension. Systemic vascular resistance is expected to be increased in hypovolemia. We used titrating doses of ketamine, as it has a sympathomimetic action which does not produce hypotension. Though the tachycardic effect due to ketamine is undesirable in these circumstances and the drug itself is a myocardial depressant in catecolamine-depleted states as in cases of shock, the options for induction of anesthesia are limited. Invasive monitoring of BP is helpful in these cases. Neither CVP monitoring nor pulmonary capillary wedge pressure can diagnose LVOT obstruction nor do these monitors give an accurate measurement of LV filling.[14]

The volatile agent causes slight myocardial depression which is useful in these patients. Episodes of hypotension can be treated with trendelenburg position, volume replacement and/or vasoconstrictors. Adequate preload should be the goal. CVP should be kept high to maintain optimal cardiac output and avoid undue increases in contractility because of hypovolemia.

Though implantable cardioverter defibrillator (ICD) implants have good outcomes during pregnancy with heart disease, medical and device complications are not uncommon.[15] These are arrhythmias, heart failure, ICD shocks and atrial lead fracture.[15] Inactivation of AICD during the intraoperative period is necessary to prevent damage to AICD by the use of cautery. However, prompt re-programming of AICD after transferring to ICU is required. This was not required in our case as bipolar cautery was used. Central venous cannulation (CVC) in a patient with an AICD is another concern. Dislodging thrombii and the risk of the guide wire of the central line getting entangled in the thrombus/clot around the pacer wires[16] is of major concern. The risk of long guide wires or the central line itself coming into contact with, and dislodging the pacemaker leads is more if placed on the ipsilateral side. We avoided the standard Seldinger guidewire technique and cannulated the left IJV with the help of a 5 cm 16 gauge I.V. cannula.[17] This was done to avoid the guide wire coiling around the pacing wire. One should avoid ipsilateral placement of CVCs in patients with permanent pacemakers on account of the possibility of thromboembolism and pacemaker malfunction due to lead displacement. Central line placement in a parturient with AICD should be done under ultrasound imaging or a C-arm with a protective shield for the fetus.[16]

SUMMARY

Management of obstetric patients with cardiac disease (HOCM with AICD in this case) is always challenging. The addition of obstetric hemorrhage in this group of the patient makes it more complex. Preoperative assessment by a team of anesthesiologists, obstetricians and cardiologists is highly desirable. All institutes should have a practice of thorough pre-anesthetic evaluation of these high-risk patients during pregnancy and before delivery. Aggressive resuscitation and timely intervention along with titration of doses of anesthetic agents, invasive monitoring, and ultrasound for CVC placement will definitely help in better outcomes.

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