A Million Picture Anesthesia for a morbidly obese

A Million $$$ Picture Anesthesia for a morbidly obese patient with severe pulmonary hypertension for robotic hysterectomy 1 Tong , 1 Stone , 1 Youngs , Chuanyao MD, Cassie DNAP, CRNA, Courtney MSNA, CRNA; Michael MD 1 -Department of Anesthesiology and 2 -Department of Obstetrics & Gynecology, Wake Forest Baptist Medical Center The case: a 43 -year old woman with recurrent AUB (abnormal uterine bleeding) Maintenance and failed IUD, also the pathology showed precancer endometrial lesion, was scheduled for robotic hysterectomy. Comorbidities: OSA, morbid obesity (BMI 61, 161 kg), chronic PE, pulmonary hypertension (PHTN), HFp. EF, HTN, DM, CHF, diastolic heart failure, anemia. PE: BP 168/89, HR 74, RR 26, Sp. O 2 98% on NCO 2 4 L. Meds: letairis, hydralazine, eliquis, Vit. C, lotensin, bumex, Vit. D, clonipine, flexeril, lovenox, iron, prozac, vistrail, insulin (55 u/d), synthroid, glucophage. Labs: WBC 4. 6, Hgb 10. 7, Plt 214; Na 136, K 4. 4, Cl 104, CO 2 26, Cr 1. 44, Glu 137; Hb. A 1 C 5. 3. ECG: SR 90, possible inferior infarction. Echocardiogram: normal LV, EF 55 -60%. LV filling pattern is prolonged, systolic and diastolic septal flattening consistent with RV volume and pressure overload. RV is moderately dilated, RV systolic function is mildly reduced. LA is mildly dilated. RA is moderately dilated. Moderate tricuspid regurgitation. Estimated right ventricular systolic pressure is 53 mm. Hg. Moderate pulmonary hypertension. The patient was seen in PAC and cleared to precede the surgery 1) Desflurane (6 -8%) and intermittent rocuronium, Ringers 150 ml/hr 2) Repeated ARMs to improve Sp. O 2 3) Epinephrine infusion was stopped shortly because of self maintained MAP Meeting the patient and her mother in holding room, additional information Understanding TMP (transmural pressure): PIP was 26 in supine and 35 in steep TP positions, and 40 when insufflated. Such a significant increase PIP is mainly caused by 1) decreased compliance of the lungs and chest, 2) the gravitation of abdominal contents, and 3) the insufflation pressure. A higher ventilator driving force is needed to ensure adequate alveoli ventilation, while the TMP remains unchanged. obtained: the patient is bed/chair bound (watching TV) most time, but she is able to take care of herself (bath, toilet, brush, clean…); chronic PE (no known the causes) on Eliquis, had syncope 6 months ago with hypoxic, most likely from her pulmonary hypertension, started NC O 2 and Viagra since then, feels much better; confirmed medications taken for Viagra and lovenox, and stopped Eliquis for 5 days. • The administration of flolan severely affect the ability to see ETCO 2, therefore, monitoring of intraoperative CO 2 was solely by ABGs (see the table). • Hypercapnia was progressively worse despite the best effort to increase mechanical ventilation with increasing ventilation rate and fresh gas flow; however, we were reluctant to dial the tidal volume up concerning iatrogenic lung injury. Hypercapnia is inevitable during robotic surgery. • Acidosis and hypercarbia could have detrimental effects on PVR in patient with severe PHTN, increasing RV afterload and decreasing LV preload. Clinically this would be manifested by worsening in metabolic acidosis, hypotension, and hypoxia. In contrast, our patient showed no signs of deteriorating in BE nor lactate acid, rather an improved oxygenation (Pa. O 2) on repeated ABGs, and a maintained MAP, indicating the patient was in a satisfied physiological condition under the anesthesia. Emergence At the end of surgery, the NMR was reversed with Sugammadex and spontaneous breathing was returned, the patient gained normal consciousness, she was extubated on the OR table, transported to PACU and was discharged to Day hospital shortly. Postoperative course Visited the patient and her mother next morning, the patient recovered well and had a good sleep overnight, was able to ambulate and the pain was minimal. Just finished her breakfast, she was ready to be discharged home and looking forward the new life. Anesthesia management If the surgery was done in a traditional way, it would take a month to recover and longer time to heal, much more of pain and suffering, plus the mounting cost to the patient and health care system-A Million $$$ Picture. Induction 1) Brought back to OR, placing the monitors, started epinephrine infusion at 3 mcg/min till increased BP over the baseline was confirmed 2) IV induction with propofol (60 + 40 +20), lidocaine 100, fentanyl 50 and establish good mask ventilation with an oral airway; IV Sux 120. DL with Glidescope, ETT was confirmed by ETCO 2 and BBS. 3) Placed an arterial line and a 2 nd iv access 4) Started inhalational Floran (epoprostenol, 0. 02 mcg/min) and heparin 5000 U/SC 5) Ventilator settings: VCV, TV 400, RR 10, PEEP 6 -8, Fi. O 2 50%; ARM (alveoli recruitment maneuver) was performed shortly due to decrease of Sp. O 2 6) Positioning took 45 min 2 Kelly , Pulmonary hypertension WHO classification: 1) idiopathic; 2) left heart diseases; 3) lung diseases or hypoxia; 4) chronic thromboembolic: recurrent PE; 5) multifactorial. Although the etiology of PHTN in this patient is not clear, it is likely multifactorial, as she has HFp. EF, recurrent PE, sleep disorder, and restrictive lung disease. Despite being moderately elevated PA pressure, the dilated RV & RA, and septal deviation, and the limitation of her functionality indicate that her pulmonary hypertension is severe, furthermore, she has been treated with Viagra and hydralazine. • • • Factors acutely ↑PVR Hypoxia Hypercapnia Acidosis ↑Sympathetic tone Exogenous or endogenous Pulmonary vasoconstrictions Pulmonary embolism Summary: successful care of this patient demonstrated 1. A strong team, good preoperative assessment and communications among the surgeons, anesthesia providers, the patient and her family member. 2. A good attitude towards challenge, and a well thought backup plan Unanswered questions 1. Should TEE and PAC be used to monitor during the surgery? 2. How do we know the administration of Flolan was beneficial? 3. Is there an upper limit for CO 2? 4. Does the respiratory acidosis have the same pathophysiological effect as metabolic acidosis? References 1. NEJM 2013; 369: 2126 -36 2. NEJM 2013; 369: 428 -31 3. Critical Care Med 2005; 9: 51 -59 4. NEJM 2004; 351: 1655 -1665