HCN4 pacemaker channels attenuate the parasympathetic response and stabilize the spontaneous firing of the sinoatrial node.

KEY POINTS: The contribution of HCN4 pacemaker channels in the autonomic regulation of the sino-atrial node (SAN) has been a matter of debate. The transgenic overexpression of HCN4 did not induce tachycardia, but reduced heart rate variability, while the conditional knockdown of HCN4 gave rise to sinus arrhythmia. The response of the SAN to ß-adrenergic stimulation was not affected by overexpression or knockdown of HCN4 channels. When HCN4 channels were knocked down, the parasympathetic response examined by cervical vagus nerve stimulation (CVNS) was enhanced; the CVNS induced complete sinus pause. The overexpression of HCN4 attenuated bradycardia induced by CVNS only during ß-adrenergic stimulation. We concluded that HCN4 pacemaker channels stabilize the spontaneous firing by attenuating the parasympathetic response of the SAN. ABSTRACT: The heart rate is dynamically controlled by the sympathetic and parasympathetic nervous systems that regulate the sinoatrial node (SAN). HCN4 pacemaker channels are the well-known causative molecule of congenital sick sinus syndrome. Although HCN4 channels are activated by cAMP, the sympathetic response of the SAN was preserved in patients carrying loss-of-function mutations of the HCN4 gene. In order to clarify the contribution of HCN4 channels in the autonomic regulation of the SAN, we developed novel gain-of-function mutant mice in which the expression level of HCN4 channels could be reversibly changed from zero to ∼3 times that in wild-type mice, using tetracycline transactivator and the tetracycline responsive element. We recorded telemetric ECGs in freely moving conscious mice and analysed the heart rate variability. We also evaluated the response of the SAN to cervical vagus nerve stimulation (CVNS). The conditional overexpression of HCN4 did not induce tachycardia, but reduced heart rate variability. The HCN4 overexpression also attenuated bradycardia induced by the CVNS only during the ß-adrenergic stimulation. In contrast, the knockdown of HCN4 gave rise to sinus arrhythmia, and enhanced the parasympathetic response; complete sinus pause was induced by the CVNS. In vitro, we compared the effects of acetylcholine on the spontaneous action potentials of single pacemaker cells, and found that similar phenotypic changes were induced by genetic manipulation of HCN4 expression both in the presence and absence of ß-adrenergic stimulation. Our study suggests that HCN4 channels attenuate the vagal response of the SAN, and thereby stabilize the spontaneous firing of the SAN.

Ectopic automaticity induced in ventricular myocytes by transgenic overexpression of HCN2.

Hyperpolarization-activated cyclic nucleotide-gated channels (HCNs) are expressed in the ventricles of fetal hearts but are normally down-regulated as development progresses. In the hypertrophied heart, however, these channels are re-expressed and generate a hyperpolarization-activated, nonselective cation current (Ih), which evidence suggests may increase susceptibility to arrhythmia. To test this hypothesis, we generated and analyzed transgenic mice overexpressing HCN2 specifically in their hearts (HCN2-Tg). Under physiological conditions, HCN2-Tg mice exhibited no discernible abnormalities. After the application of isoproterenol (ISO), however, ECG recordings from HCN2-Tg mice showed intermittent atrioventricular dissociation followed by idioventricular rhythm. Consistent with this observation, 0.3 µmol/L ISO-induced spontaneous action potentials (SAPs) in 76% of HCN2-Tg ventricular myocytes. In the remaining 24%, ISO significantly depolarized the resting membrane potential (RMP), and the late repolarization phase of evoked action potentials (APs) was significantly longer than in WT myocytes. Analysis of membrane currents revealed that these differences are attributable to the Ih tail current. These findings suggest HCN2 channel activity reduces the repolarization reserve of the ventricular action potential and increases ectopic automaticity under pathological conditions such as excessive ß-adrenergic stimulation.

[A Case of Postoperative Paraplegia Caused by Idiopathic Spinal Cord Infarction following Hepatectomy under Both General and Epidural Anesthesia].

A 73-year-old woman (height : 155 cm, weight : 55 kg) was scheduled to undergo a laparotomic hepatectomy and radiofrequency ablation for hepatocellular carcinoma. Her medical history did not include any relevant conditions such as cardiovascular or neurological disorders. A thoracic epidural catheter was introduced at T8-9 before the induction of anesthesia with intravenous propofol. General anesthesia was maintained with the inhalation of oxygen, air, and desflurane, and the continuous infusion of remifentanil. Several intraoperative episodes of mild hypotension occurred, each of which was successfully treated with intravenous ephedrine, but otherwise her anesthetic course was uneventful, and she recovered from the anesthesia smoothly. Her postoperative pain was well controlled with continuous epidural infusion of levobupivacaine and fentanyl, and she could walk by herself on postoperative day (POD) 1. However, she suffered weakness in her lower extremities on POD2 and subsequently fell into complete paraplegia with sensory loss below the T4 level on POD3. A magnetic resonance imaging scan taken on POD4 showed an idiopathic spinal cord infarction (SCI) involving levels T1 through T4, although no epidural abnormalities, e.g., hematomas, were detected. Immediate treatment with methylprednisolone, ozagrel, and edaravone failed to resolve her symptoms. We suggest that it is of great importance to consider SCI as a differential diagnosis as soon as possible in cases of unanticipated postoperative paraplegia.

Efficient transduction of 11 poly-arginine peptide in an ischemic lesion of mouse brain.

Direct intracellular delivery of intact proteins has been successfully achieved by tagging cell-penetrating peptide (CPP), which consists of short positively charged amino acids, such as 11 poly-arginine (11R); however, in vivo delivery of the proteins to the brain has remained challenging because it is unclear whether CPP would enable proteins to cross the blood-brain barrier (BBB). In this study, we conducted an in vivo kinetic study to investigate the efficiency of 11R-mediated peptide delivery in the normal and ischemic brain. The 11R was observed in the microvessels and neurons surrounding the microvessels throughout the brain 1 hour after systemic administration, but the signal of the peptide was faint after 2 hours. In a transient middle cerebral artery occlusion mouse model, 11R was markedly enhanced and remained detectable in the cells on the ipsilateral side for as long as 8 hours after administration compared with the contralateral side. These results suggest that 11R is capable of in vivo delivery to the brain by passing through the BBB. Furthermore, 11R-mediated protein transduction could be used for the delivery of therapeutic molecules in cerebral ischemia.

[Combined spinal-epidural anesthesia for a patient with HTLV-1 associated myelopathy].

An 81-year-old female with HTLV-1 associated myelopathy (HAM) was scheduled for transurethral lithotomy. She had had paresthesia and spastic paresis in the lower extremities for the past 15 years. The preoperative respiratory function test revealed a vital capacity of 1.3 l (58% of the predicted value). We selected combined spinal-epidural anesthesia (CSEA) for her to avoid postoperative respiratory complications due to general anesthesia. After placement of a thoracic epidural catheter, spinal anesthesia was achieved by administration of bupivacaine 7.5 mg, resulting in the sensory block level to T 6, five min later. The intraoperative blood pressure remained high at 150-200 mmHg, in spite of the administration of nicardipine. Postoperatively, neither the deterioration in the neurological findings of HAM nor the exacerbation of respiratory function was observed. The present report suggests that CSEA can be one of the choices of anesthesia for a patient with HAM.

[Anesthetic management of a patient with Trousseau's syndrome and ovarian cancer who underwent gynecological surgery].

Trousseau's syndrome, a complex paraneoplastic disease, is characterized by the occurrence of thromboembolic disorders such as brain infarctions in patients with malignant neoplasms. We report the case of a 46-year-old woman with ovarian cancer who had suffered cerebral infarctions and presented with left hemiplegia, aphasia, and atypical genital bleeding. She suffered multiple right brain infarctions, a pulmonary embolism, a right renal infarction with bilateral hydronephrosis and deep venous thromboses and exhibited increased D-dimer and fibrinogen levels and so was administered heparin (10,000 U x day(-1)). She had no other underlying diseases such as coagulopathy, cardiovascular disease, collagen disease, or angiitis. Therefore, we were able to diagnose her with Trousseau's syndrome. She was scheduled to undergo total abdominal hysterectomy with bilateral oophorectomy, pelvic lymphadenectomies, and omentectomy. Preoperatively, an inferior vena cava filter was temporarily installed to prevent the development of further pulmonary thromboses. General anesthesia was uneventfully maintained by inhalation of oxygen, air, and sevoflurane and the continuous infusion of remifentanil whilst regional cerebral oxygen saturation and transesophageal echocardiography monitoring were performed. Postoperatively, she received heparin-based anticoagulant therapy (10,000 U x day(-1)) and did not exhibit bleeding diathesis or thrombosis. It is of great importance that anesthesiologists are aware of the thromboembolic status of patients with malignant neoplasms, especially those with gynecological tumors.

[A case of ventricular tachycardia that was probably caused by coronary artery spasm induced by pericardial manipulation].

We present a case of ventricular tachycardia (VT) that was probably caused by coronary artery spasm. A 74-year-old man was scheduled to undergo right lower lobectomy for lung cancer. Although he had never suffered from any episodes of ischemic heart disease, he had several risk factors for coronary artery disease (CAD); i. e., a history of smoking, a low high-density lipoprotein cholesterol level, and diabetes mellitus type 2. Anesthesia for one-lung ventilation was maintained by inhalation of sevoflurane (1-1.5%), the continuous intravenous infusion of remifentanil (0.1-0.15 µg x kg(-1) x min(-1)), and the intermittent administration of epidural (T4-5) 2% mepivacaine (4 ml) and 0.75% ropivacaine (5 ml). During manipulation of the pericardium, the patient's systolic blood pressure suddenly increased to 200 mmHg, followed by an ST elevation on his electrocardiogram. Despite the immediate infusion of nitroglycerin (1 mg), he developed non-sustained VT, lasting for about 30 seconds. Then, diltiazem (0.5 µg x kg(-1) x min(-1)) was continuously administered, and the infusion rate of remifentanil was increased to 0.3 µg x kg(-1) x min(-1). The patient recovered smoothly from anesthesia and his postoperative course was uneventful. Anesthesiologists should be aware of the possibility of coronary artery spasms induced by sudden modulation of the autonomic nervous system, particularly in patients who are at high risk of CAD.

A case of delayed emergence from anesthesia caused by postoperative brain edema associated with unexpected cerebral venous sinus thrombosis.

Cerebral venous sinus thrombosis (CVST) is rare but displays various and often dramatic clinical symptoms. Few cases of CVST have been reported in the field of anesthesiology. We encountered an unexpected case of CVST that presented with delayed emergence from anesthesia after resection of a brain tumor. A 55-year-old man was scheduled for resection of an oligoastrocytoma in his right frontal lobe. After smooth induction of general anesthesia, anesthesia was maintained uneventfully for about 7 h with target-controlled infusion (TCI) of propofol and remifentanil, except for a seizure generated when the right anterior central gyrus was stimulated to allow motor evoked potential monitoring. Immediately after the cessation of TCI, spontaneous respiration was restored. However, the patient was unexpectedly comatose, and no response to painful stimuli or coughing during tracheal suctioning was observed. A computed tomogram taken 2 h after surgery showed diffuse brain edema, even though the neurosurgeons did not notice any cerebral swelling during closing of the dura mater. A magnetic resonance venogram revealed thromboses in the superior sagittal and straight sinuses. On the 9th postoperative day, the patient died without recovering consciousness or his brainstem reflexes. Anesthesiologists should be aware of CVST as a cause of delayed emergence from anesthesia after craniotomy.

[A case of a giant ovarian cyst anesthetized with the use of an inferior vena cava filter].

An intraperitoneal giant tumor can form deep venous thrombosis (DVT), leading to pulmonary embolism (PE) when it is removed. We report a case of a giant ovarian cystic tumor with possible DVT. A 52-year-old woman (149 cm in height, 85 kg in weight, and 150 cm in ventral girth) underwent the laparoscopic resection of the cyst. Preoperative angiography showed the obstruction of the inferior vena cava (IVC) just below the level of the right renal vein due to the compression by the tumor, and computed tomography suggested the existence of distal DVT. Anesthesia was induced with propofol and fentanyl, and the trachea was intubated using rocuronium. A permanent type IVC filter was placed near the obstruction site to prevent PE. Transesophageal echocardiography (TEE) was employed to detect the thrombotic echogram at the right atrium. Anesthesia was maintained with inhalation of sevoflurane and intravenous infusion of remifentanil. The content of the cyst (40.5 l) was suctioned slowly in about 50 min to avoid reexpansion pulmonary edema and circulatory collapse. Neither thrombotic echogram nor the acute decrease in end-tidal carbon dioxide pressure was observed throughout the anesthesia. Operation was performed uneventfully, and she recovered from anesthesia. We consider that IVC filters and TEE are useful to manage surgical patients with a huge ovarian cyst.

Postoperative neurological complications and risk factors for pre-existing silent brain infarction in elderly patients undergoing coronary artery bypass grafting.

PURPOSE: Elderly patients with multiple infarctions revealed a high prevalence of postoperative stroke after coronary artery bypass grafting (CABG). However, postoperative neurological complications and characteristics of silent brain infarction (SBI) have not been evaluated in elderly patients undergoing CABG. METHODS: Four hundred forty-nine patients (≥60 years old) scheduled for CABG underwent cerebral magnetic resonance imaging (MRI) and MR angiography preoperatively to assess cerebral infarctions and carotid and intracranial artery stenosis. Atherosclerosis of the ascending aorta was assessed by epiaortic ultrasound during surgery. Patients were sorted by their history of cerebrovascular disease (CVD) and the presence of infarction by MRI: SBI (infarction without CVD), BI (symptomatic brain infarction; CVD and infarction), and controls (no findings of either CVD or infarction). RESULTS: SBI was found in 35.5% of the 449 patients and increased with age. The prevalence of pre-existing multiple infarctions was less frequent in SBI than in BI. The incidence of postoperative stroke and cognitive dysfunction was 1.3% and 4.9% in controls (n = 225), 5.7% and 15.2% in SBI (n = 158), and 9.1% and 18.2% in BI (n = 66). Patients with SBI were older and had more renal dysfunction and preoperative cognitive impairment. Stepwise logistic regression demonstrated that age, renal dysfunction, preoperative cognitive impairment, atherosclerosis of the ascending aorta, and intracranial arterial stenosis were associated significantly with SBI. CONCLUSION: Patients with SBI were ranked at moderate risk of neurological complications after CABG between control and BI. Increased age, renal dysfunction, and preoperative cognitive impairment appeared to be strongly associated with SBI.

[Anesthetic management of a patient with Rett syndrome associated with trismus and apnea attacks].

Rett syndrome (RTT) is a congenital neurological disorder associated with mutations in the gene encoding MECP2 on the X chromosome. An 18-year-old woman (150 cm in height and 29 kg in weight) had been diagnosed with RTT and showed myotonic trismus, frequent attacks of apnea, mental retardation, spastic paraplegia, scoliosis, and microcephalus with micrognathia. She was scheduled to undergo laparoscopic fundoplication and gastrostomy under general anesthesia. Nasal bronchofiberscopic intubation (BFI) was planned because difficult airway due to trismus and micrognathia was expected. Referring to the bispectral index (BIS), anesthesia was induced with intermittent intravenous thiopental (total 125 mg), resulting in successful opening of the mouth by 1.5 of a finger width and establishment of manual ventilation. Following intravenous administration of rocuronium (20 mg), oral BFI was easily accomplished despite Cormack grade III. Anesthesia was satisfactorily maintained with inhalation of sevoflurane (1.0-1.5%) and continuous infusion of remifentanil (0.1-0.2 microg x kg(-1) x min(-1)) with the BIS value ranging from 30 to 50. She recovered smoothly from anesthesia using sugammadex (50 mg). However, she immediately demonstrated trismus and an attack of apnea with shivering, which were successfully resolved by warming the body and intravenous fentanyl (50 microg bolus and subsequent infusion at a rate of 10 microg x hr(-1)). The postoperative course was uneventful. Characteristically, RTT shows an extremely wide range of neurological symptoms. Therefore, it is of great importance to respond to each of those symptoms during the perioperative management of patients with RTT.

Prognostic factors associated with mortality in patients undergoing emergency surgery for abdominal aortic aneurysms.

PURPOSE: Surgical mortality rates following emergency surgery for ruptured abdominal aortic aneurysms (AAAs) remain high. This study investigated the mortality rate and identified prognostic factors affecting mortality in patients undergoing emergency repair of AAAs in our hospital. METHODS: Between January 2005 and June 2010, a total of 42 patients underwent emergency surgery for AAAs and were included in this retrospective study. The following variables concerning each patient were collected by chart review and compared between survivors and nonsurvivors: age; gender; preoperative levels of hemoglobin (Hb), hematocrit (Ht), platelets (Plts), base excess (BE), and serum glucose and lactate; presence of preoperative shock defined as hypotension (systolic blood pressure of less than 80 mmHg); incidence of blood transfusion, whether AAA was ruptured or impending; interval from admission to the hospital or arrival in the operating room until aortic cross-clamping; surgical duration; and volume of intraoperative blood loss and transfusion, total fluid infusion, and urine output. RESULTS: Nine patients died within 30 days postoperatively, a 30-day mortality rate of 21.4%. Among these nine nonsurvivors, eight had shown persistent preoperative shock (P = 0.0004 vs. survivors). Compared with the survivors, nonsurvivors were significantly older (P = 0.0052) and had lower preoperative levels of Hb/Ht (P < 0.0001), Plts (P = 0.0003), and BE (P < 0.0001), an elevated lactate level (P = 0.0048), shorter interval from admission (P = 0.0459) or arrival in the operating room (P = 0.0288) until aortic clamping, and intraoperatively more hemorrhage (P = 0.0038) associated with larger amounts of blood transfusion (P = 0.0083) and less urine output (P = 0.0004). CONCLUSIONS: The authors clarified that certain features such as age, persistent preoperative shock, and greater amounts of transfusion associated with greater blood loss and anemia were factors affecting the mortality in patients undergoing emergency surgery for AAAs. It might be of great importance to correct preoperative shock and anemia caused by massive bleeding before the onset of hemodynamic deterioration.

A case of nonsustained ventricular tachycardia immediately following modified electroconvulsive therapy in a depressive patient.

Modified electroconvulsive therapy (mECT) with the use of hypnotics and muscle relaxants is an optional and prevailing treatment for depression in patients who have failed on antidepressant regimens. We describe a patient who developed ventricular tachycardia (VT) immediately after mECT. A 64-year-old man with no remarkable past history underwent a course of mECT for drug-resistant depression. Anesthesia was induced with intravenous thiopental (150 mg) followed by rocuronium (50 mg). Three minutes after the administration of rocuronium, the brain was electrically stimulated using a pulse wave. The first mECT session was performed uneventfully. However, the second session 2 days later elicited acute hypertension (182/134 mmHg) and tachycardia (130 bpm), resulting in the appearance of single and couplets of premature ventricular contractions on the electrocardiogram followed by VT lasting about 10 s. The chest was immediately compressed several times, then normal sinus rhythm was spontaneously restored without administering antiarrhythmic agents. The patient recovered from anesthesia without complications. Postoperatively, close examination was unable to definitively determine the cause of VT, resulting in the cancellation of subsequent mECT sessions. It is important to bear in mind that mECT can induce life-threatening arrhythmias such as VT.

A case of serious laryngeal edema unpredictably detected during laryngoscopy for orotracheal intubation following induction of anesthesia.

We report a case of unpredictable and serious laryngeal edema probably caused by preoperative esophagogastroduodenoscopy (EGD). A 54-year-old man with type 2 diabetes mellitus was scheduled to undergo coronary artery bypass grafting (CABG). Two days before surgery, EGD was performed to explore the cause of occult bleeding, resulting in a slightly sore throat and an increased white blood cell count (18,300/µl). Without premedication, general anesthesia was uneventfully induced with intravenous midazolam (10 mg) and fentanyl (50 µg), followed by inhalation of sevoflurane (3%) and intravenous rocuronium (50 mg). Thereafter, manual ventilation was easily performed with a bag and mask. However, on laryngoscopy for orotracheal intubation, serious swelling with rubor and light pus in the epiglottis extending to the arytenoid cartilage was detected, leading to the cancellation of surgery. Immediately following intravenous drip of hydrocortisone (300 mg) and bolus of sugammadex (200 mg), the patient recovered smoothly from anesthesia without complications such as dyspnea, but his sore throat persisted. He was diagnosed with acute epiglottitis. Treatment consisted of intravenous cefazolin (2 g/day) and hydrocortisone (300 mg/day tapered to 100 mg/day) for 9 consecutive days. Consequently, the patient recovered gradually from the inflammation and underwent CABG as scheduled 28 days later. Anesthesiologists should be aware that EGD performed just before anesthesia could unpredictably cause acute epiglottitis, especially in immunocompromised patients, such as those with diabetes.

[Recovery from rocuronium by sugammadex does not affect motor evoked potentials].

Motor evoked potential (MEP) monitoring has been employed to detect the spinal cord injury during spinal, neurosurgical and cardiovascular operations. Muscle relaxants diminish the amplitude of MEP because MEP is the picture of electromyogram. In 5 cases undergoing MEP monitoring, we examined the effect of rocuronium followed by the administration of sugammadex on MEP Anesthesia was induced with propofol (target controlled infusion 3.0-3.5 microg x ml(-1)) and remifentanil 0.15-0.3 microg x kg(-1) x min(-1), and the trachea was intubated with the use of rocuronium 0.6 mg x kg(-1) without any muscle rigidity, bucking and laryngospasm. General anesthesia was maintained by total intravenous anesthesia using propofol and remifentanil with no muscle relaxants. Immediately after the tracheal intubation, sugammadex 4 mg x kg(-1) was intravenously given. The amplitude of MEP was measured just before the administration of rocuronium, immediately after the tracheal intubation, and 1, 2, 3, 5 min following the administration of sugammadex. Sugammadex restored the MEP amplitude, deteriorated by rocuronium, in 3 to 5 min to the level of non-paralytic muscles. In one case, it took 8 min to restore the MEP of hemiparetic leg. Taking these findings into consideration, it is likely that rocuronium might not affect the MEP when reversed by sugammadex, and should be safe for smooth tracheal intubation in patients who need MEP monitoring.

[Factors that affect the mortality in patients receiving emergency surgery for ruptured abdominal aortic aneurysms].

This retrospective study was performed to identify the perioperative factors affecting the mortality rate in 28 patients, who had received emergency surgery for ruptured abdominal aortic aneurysms from January, 2005 to June, 2008. Five (17.9%) of these 28 patients died of massive bleeding, sepsis, or multiple organ failure during or within 11 days after surgery. Various factors which might influence the outcomes were compared between the survivors and non-survivors. Preoperative hypotension defined as a systolic blood pressure < or = 80 mmHg associated with hemorrhagic shock was the only significant factor affecting the mortality. There were no significant differences in age, gender, the time from the admittance to the hospital to aortic cross clamping, duration of surgery, and the amount of blood products transfused and intraoperative blood loss, between the two groups. Of great importance is that preoperative hypotension should be corrected before the onset of hemodynamic deterioration.

[Case of possible transfusion-related acute lung injury during thoracic endovascular aortic repair].

Transfusion-related acute lung injury (TRALI) is a serious complication of blood transfusion, which is characterized by the acute onset of non-cardiogenic pulmonary edema and hypoxemia following the administration of blood products. We report a case of possible TRALI during thoracic endovascular aortic repair (TEVAR). The patient was a 61-year-old man (161 cm in height, 61 kg in weight) who underwent TEVAR for the traumatic injury at the isthmus of aorta. He had a light preexisting lung injury. About 1 hour following the blood transfusion (red cell concentrates, fresh-frozen plasma, and platelet concentrates), he suddenly fell into severe hypoxemia (PaO2 52 mmHg in FI(O2) of 1.0). The radiographic examination showed pulmonary edema, i. e., bilateral infiltrates and pleural effusion. No evidence of circulatory overload was observed. Anti-human leukocyte antigen antibodies in his serum and anti-granulocyte antibodies in the donor blood were detected. In spite of intensive care including artificial ventilation with positive end-expiratory pressure and the administration of methylprednisolone and a granulocyte elastase inhibitor, he died of exacerbated hypoxemia and hypotension 4 hours after the onset of acute lung injury. Of great importance is being aware of an unexpected occurrence of TRALI during and soon after blood transfusion.

Anesthetic management during a cesarean section in a patient with cleidocranial dysplasia: a case report.

BACKGROUND: Cleidocranial dysplasia is a type of skeletal dysplasia, which is primarily characterized by delayed ossification of skeletal structures. It causes facial and oral abnormalities, resulting in difficult airway management and neuraxial anesthesia. CASE PRESENTATION: The patient was a 24-year-old primipara (height 138 cm, weight 42 kg) with a hypoplastic right clavicle, patent fontanelles, dental malalignment, and a high palate. She was diagnosed with cleidocranial dysplasia at birth, although gene examination has not been performed. The fetus was confirmed to have short limbs and large fontanelles during an examination performed at 28 weeks gestation, suspected to have cleidocranial dysplasia. The mother was scheduled for a cesarean section at 37 weeks and 1 day due to cephalopelvic disproportion. Preoperative radiography and magnetic resonance imaging revealed no vertebral and spinal abnormalities, which allowed combined spinal-epidural analgesia (CSEA) to be performed. The surgery was safely concluded under CSEA with no intraoperative respiratory or circulatory problems. CONCLUSIONS: Patients with cleidocranial dysplasia exhibit facial, oral abnormalities, and often vertebral abnormalities. Imaging assessments before neuraxial anesthesia and careful preparation for airway management are required.

Anesthetic Management of Pleurectomy/Decortication Under Differential Lung Ventilation.

A 64-year-old male (a building demolition worker) was diagnosed with malignant left-sided pleural mesothelioma, and left-sided pleurectomy/decortication was scheduled. Differential lung ventilation (DLV) was performed during the removal of the visceral pleura by connecting the affected lung to a ventilator and the healthy lung to an anesthesia machine, and then separately ventilating the left and right lungs. Anesthetic management using DLV was successfully established without causing significant changes in oxygenation or circulatory dynamics.