http://dx.doi.org/10.7570/kjo.2012.21.3.183 □ CASE REPORT □
- 183 - Introduction
Obesity is a complex and multifactorial disease which is associated with an increased incidence of a wide spectrum of medical and surgical pathologies. Surgical therapy should be considered for individuals who have a body mass index (BMI) greater than 40 kg/m
2or have a BMI greater than 35 kg/m
2with significant co-morbidities and show that dietary attempts at weight control have been ineffective.
1)However, surgery and anesthesia can both lead to impaired lung function, abnormal gas exchange and respiratory mechanics which in turn may lead to postoperative respiratory complications.
2)We report a case of a super morbid obese patient who presented with acute hypercapnic respiratory failure immediately after bariatric surgery
Case Report
A 37-year-old female with height 145cm and weight 135 kg (BMI > 64 kg/m
2) was scheduled for laparoscopic sleeve gastrectomy. She had no medical or surgical history except for newly diagnosed diabetes mellitus. The patient denied history of obstructive sleep apnea and has New York Heart Association functional class III.
Transthoracic echocardiography revealed enlarged heart
복강경하 위소매 절제 술 후 발생한 고이산화탄소 혈증을 동반한 호흡 부전-증례보고
Hypercapnic Respiratory Failure Immediate After Bariatric Surgery
조윤이․정월선․박희연․장영진
*가천대학교 길병원 마취통증의학과
Youn Yi Jo, Wol Seon Jung, Hee Yeon Park, Young Jin Chan
*Department of Anesthesiology and Pain Medicine, Gachon University Gil Medical Center
요 약
흉부나 상복부 수술과 이에 동반한 전신마취는 일시적인 가 스교환의 이상과 부적절한 호흡역학을 동반한 폐기능 장애가 수반될 수 있으며 이는 비만한 환자에서 더 심각하게 나타날 수 있다. 비만 저환기 증후군을 가진 37세 여환이 복강경 하 위소매절제술을 시행받았다. 환자는 복강경 수술을 위한 복강 내 이산화탄소 주입 후 교정되지 않는 심각한 호흡성 산증이 있었고, 술 후 각성 후 고이산화탄소 혈증을 동반한 호흡 부전 을 경험하였다. 이에 저자들은 비만환자들의 수술 및 마취 중 나타나는 생리적 변화에 대한 중요성을 인식하고 가능한 합병 증에 대하여 참고문헌과 함께 기술하였다.
중심단어: 비만, 비만 저환기 증후군, 전신 마취
ABSTRACT
Surgery and general anesthesia can both lead to impaired lung function, abnormal gas exchange and abnormal respiratory mechanics in obese patients. A 37 year old obese female who had obesity hypoventilation syndrome underwent laparoscopic sleeve gastrectomy. She experienced hypercapnic respiratory failure during and after the operation period. It is important to recognize the pathophysiologic changes of obesity and prepare for the possible complications during anesthesia and surgery of obese patients.
Key words: Obesity, Obesity hypoventilation syndrome, Anesthesia
ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ
Received: Jun. 19, 2012; Reviewed: Jul. 10, 2012; Accepted: Sep. 5, 2012
Corresponding author: Young Jin Chang, Department of Anesthesiology and Pain Medicine, Gachon University of Medicine and
Science Gil Medical Center, 1198 Guwol-dong, Namdong-gu, Incheon 405-760, KoreaTel: 82-32-460-3637, Fax: 82-32-469-6319, E-mail: yjsk@gilhospital.com, Mobile: 010-7121-9064
－ The Korean Journal of Obesity Vol. 21, No. 3, 2012 －
- 184 - chambers without regional wall motion abnormality. Left ventricular ejection fraction was 60% and right ventricular systolic pressure was 47 mmHg. Spirometry showed a forced vital capacity (FVC) of 1.55 L (54% of reference), forced expiratory volume in 1 second (FEV
1) of 1.29 L (57%) and FEV
1/FVC of 83%. All other Biochemistry values were within normal limits except for high glucose level (fasting blood sugar 111 mg/dL, HbA1C 7.1%).
Chest X-ray showed cardiomegaly with no active lung lesion. She was not premedicated upon arrival at the operating room and standard monitoring devices were applied. Vital signs were 156/85 mmHg, 94 beats/min, and SpO
2revealed 94% before anesthetic induction. After preoxygenation, anesthesia was induced with 150 mg of propofol and 80 mg of rocuronium. Tracheal intubation was performed using a single lumen internal diameter (ID) 7.0 mm endotracheal tube in one attempt without difficulty. Bilateral breathing sounds were confirmed by auscultation and there were no wheezing or adventitious sound. Anesthesia was maintained with desflurane and remifentanil and adjusted to maintain a bispectral index (BIS) score between 40 and 60. Compression stocking and intermittent pneumatic compression device were applied
on both legs for preventing deep vein thrombosis.
Patient’s lungs were ventilated with a pressure controlled ventilation with peak inspiratory pressure at 35 cm H
2O, positive end-expiratory pressure 5 cm H
2O at a respiratory rate of 16~18 breaths/min in 100% oxygen. SpO
2was maintained within 94~96% and end tidal CO
2was 48~53 mmHg. Nicardipine was infused to control high blood pressure. The procedure lasted for 4 hours in reverse Trendelenburg position. There were no event of subcutaneous emphysema or bronchial secretion retention.
Supplemental neuromuscular blocking agent was not used during the operation. At the end of surgery, all anesthetic agents were discontinued and the residual neuromuscular blockade was reversed with pyridostigmine and glycopyrrolate. The tracheal tube was removed after smooth endotracheal and oral suction, when the patient responded to verbal commands, and showed sufficient spontaneous respiration and neuromuscular function. The patient remained in the post-anesthetic care unit for 2 hours due to persistant uncompensated respiratory acidosis even in alert mental state. The patient’s vital signs were 128/56~145/78 mmHg, 79~90 beat/min, 16-18 breaths/min with encouraged deep breathing, and SpO
2of 96% with
Fig. 1. A. Preoperative chest postero-anterior view showed cardiomegaly with no active lung lesion. B. On postoperative day 1, mild
pulmonary edema was revealed in chest antero-posterior view.Table 1. Perioperative arterial blood gas analysis
pH PaCO2
(mmHg) PaO2 (mmHg) HCO3
(mEq/L)
SaO2
(%)
FiO2
(%)
Preop 7.407 46 70.6 29.2 93.8 0.21
Induction 5 min 7.37 58 57 33.5 88 1.0
OP 1 h 7.36 54 87 30.5 96 1.0
OP 2 h 7.32 57 107 29.4 98 1.0
OP 3 h 7.27 62 94 28.5 96 1.0
OP 4 h 7.2 80 99 31.3 96 1.0
PACU 1 h 7.27 63 147 28.9 99 0.6
PACU 2 h 7.296 60.6 118.8 29.8 98 0.6
POD 1 7.283 72.5 91.9 34.6 95.5 0.3
PACU, post-ansthetic care unit; POD, Postoperative day.
－ Hypercapnic Respiratory Failure Immediate After Bariatric Surgery －
- 185 - 10L supply of oxygen through O
2mask. Postanesthesia recovery score was 9 and she was transferred to the intensive care unit for possibility of apnea and monitoring of oxygenation. Patient was closely monitored and physiotherapy was continued. The respiratory acidosis was not aggravated and follow up chest x-ray (Table 1, Fig.1) revealed mild pulmonary edema without complication.
The patient was therefore transferred to the general ward with stable vital signs (130/88~156/99 mmHg, 82~97 beat/min, 16~20 breaths/min, SpO
295~98% with nasal cannula O
23L) on postoperative day 1. She had an uneventful recovery and was discharged on postoperative day 3.
Discussion
We described a case of hypercapnic respiratory failure immediately after bariatric surgery.
In obese patients, reduction in total lung capacity, vital capacity, functional residual capacity and increase in residual volume have been described. Patients with more upper fat distribution tend to have more severe reduction in lung volume.
3)The patient in our case report showed derangement of lung mechanics in preoperative spirometry. Furthermore, fat accumulation around ribs and diaphragm, and intraabdominal tissue reduce the chest wall compliance. During general anesthesia, most of the patients experience atelectasis and these changes are greater in obese patients.
4)Laparoscopic procedures also aggravate these problems, pneumoperitoneum with CO
2gas insufflation enhances the increased intra abdominal pressure, restriction of diaphragmatic movement, and systemic absorption of CO
2gas.
5)In our patient, although we applied PEEP in reverse Trendelenburg position, she experienced persistant desaturation and hypercapnic events with high airway pressure. Based on the Bohr equation, dead space ventilation/tidal volume increased up to 51%
during the operation in our patient. The increase in dead space can usually be counteracted by increasing minute ventilation. However, we failed to reduce the dead space ventilation considering the excessive airway pressure.
Obesity hypoventilation syndrome is defined as a combination of obesity (BMI > 30 kg/m
2), awake arterial hypercapnia (PaCO
2> 45 mmHg) and absence of other known causes of hypoventilation.
6)Compared with the obstructive sleep apnea, patients with obesity
hypoventilation syndrome have day time hypercapnia and hypoxia, which are associated with pulmonary hypertension and right side congestive heart failure.
7)Patients with obesity hypoventilation syndrome blunted in both hypercapnic and hypoxemic ventilator responses.
They seem to lack the compensatory ability to increase central ventilator drive to hypercapnia.
8)Sometimes obesity hypoventilation syndrome is under-recognized and under-treated and could lead to high mortality and morbidity.
5)The preoperative arterial blood gas analysis of our patient was suitable for the definition of obesity hypoventilation syndrome and after emergence, hypercapnia was persisted even in alert mental state. In this situation, continuous or bilevel positive airway pressure is the treatment of choice.
6)Although supplemental oxygen alone is inadequate, we did not apply the positive airway pressure after emergence, because the patient could not tolerate the non-invasive mechanical device.
Obesity itself inhibits respiratory muscle function and can predispose to CO
2retention. Although hypertension and tachycardia commonly occur during hypercapnia, they may not be seen in postsurgical patients who have an attenuated response to increased CO
2level.
9)Our patient was alert and could breathe deeply and cough. Although hypercapnia with respiratory acidosis was persistent, our patient did not fulfil the reintubation criteria. Criteria for considering reintubation includes an increase in PaCO
2>
10 mmHg, decrease in pH > 0.1, PaO
2< 60 mmHg or SaO
2< 90% while supplying FiO
2> 0.5, increased signs of respiratory work and inability to protect the airway due to upper airway obstruction with excessive secretion.
10)In the morbidly obese patient, bariatric surgery is very
effective for weight reduction. Bariatric surgery may
gradually increase as the incidence of obesity is
increasing. The patient with obesity hypoventilation
syndrome has higher rate of intensive care unit admission
(40% vs. 6%)
11)and mortality rate (23% vs. 9%)
compared with patients with similar degree of obesity but
without hypoventilation.
12)Therefore, it is important to
recognize the pathophysiologic changes of obesity and
prepare for possible complications such as excessive dead
space ventilation with decreased lung volume, abnormal
respiratory drive and difficulty intubation during
anesthesia and surgery in these patients. Preparing the
monitoring system, ICU and ventilator is necessary in
－ The Korean Journal of Obesity Vol. 21, No. 3, 2012 －
