Cytokine response in cerebrospinal fluid after birth asphyxia

Experimental studies suggest that cytokine-mediated inflammatory reactions are important in the cascade leading to hypoxic-ischemic brain injury. The purpose was to study the content of pro- and antiinflammatory cytokines in cerebrospinal fluid (CSF) of asphyxiated and control infants. Samples of CSF were obtained from 20 infants who fulfilled the criteria of birth asphyxia and from seven newborn control subjects. The concentrations of IL-1beta, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, and granulocyte/monocyte colony-stimulating factor (GM-CSF) were determined with ELISA and of IL-6 using a bioassay. The concentration of IL-6 (pg/mL) was higher in asphyxiated (250, 35-543; median, interquartile range) than in control (0, 0-18) infants (p = 0.001). There was also a significant relationship between IL-6 and the degree of HIE, and between IL-6 and outcome. In addition, the content of IL-8 (pg/mL) was higher (p = 0.009) in the asphyxia group (170, 70-1440), than in the the control group (10, 0-30) and there was an association between IL-8 and degree of HIE. The levels of IL-10, TNF-alpha, GM-CSF, and IL-1beta did not differ between groups. In conclusion, the proinflammatory cytokines IL-6 and IL-8 were markedly elevated in CSF of asphyxiated infants, and the intrathecal levels of these cytokines corresponded to the degree of HIE.     

Diagnosis of drowning by combined computer-assisted histomorphometry of lungs with blood strontium determination

The aim of our study was to examine the combined contribution of computer-assisted histomorphometry of lungs with blood strontium (BS) measurement to the diagnosis of drowning in cadavers recovered from fresh water. The study population comprised 116 drowned subjects. The results for this group were compared with those obtained for three non-drowned groups: 22 subjects who died from causes other than asphyxia, 13 subjects who died of asphyxia (strangulation or hanging); and 23 healthy living subjects in whom normal BS level was measured. Samples of water where the bodies had been found were analyzed in order to establish a relation with the BS concentration of the drowned subjects. Histologically, each type of pulmonary lesion (congestion, edema, alveolar macrophages, alveolar hemorrhage, and emphysema aquosum) was evaluated semiquantitatively using a score according to the severity of the pathology. Then, a quantitative histomorphometric study was performed using a computer-assisted image analyzer to measure the length and thickness of the alveolar walls, and the area and density of the alveolar cavities. The mean values of the BS levels in the 116 drowned subjects and of the water strontium concentrations were found to be much higher than in the living individuals. Although the ranges were wide, we found no overlap between values found in drowned subjects and those in non-drowned subjects. Emphysema aquosum and to a lesser extent alveolar hemorrhage were found to be the most significant histologic changes in the drowned and asphyxia groups compared with the nonasphyxia control groups.     

Significance of intrapartum asphyxia for the onset of fetal brain damage

The prevalence of cerebral palsy is around 0.2% and has remained constant during the last 30 years. Retrospective case-control studies do not show a clear correlation between perinatal asphyxia and the development of cerebral palsy. Less than 10% of all cerebral palsy cases show signs of severe asphyxia during labour and delivery as the major pathological and likely cause for the brain damage. Severe cases of birth asphyxia with multiorgan defects and signs of hypoxic-ischaemic encephalopathy have a high mortality and the risk of permanent brain damage is increased by a factor of 10 to 30. Inspite of this, 90% of the survivors show normal development. The association between perinatal asphyxia and neuromotor developmental disturbances does not provide proof of a causal connection. Intrapartal abnormalities of foetal heart rate monitoring are not specific for foetal asphyxia and show only a limited correlation with the apgar and the cord blood pH. Foetal heart rate recording with pathological changes does not imply an elevated risk of later problems with neuromotor development and the widespread use of foetal heart rate monitoring during labour and delivery did not result in a significant reduction in the frequency of cerebral palsy. In addition to malformations, various forms of antinatal pathology like prematurity, intrauterine growth retardation and congenital infections are related to the development of brain damage. In each case of birth asphyxia, additional pathology like congenital infections or malformations in addition to changes in brain structure as a result of asphyxia must be ruled out using specific diagnostic methods like ultrasound, computed tomography and magnetic resonance. Furthermore, a careful documentation of the developmental phases is of fundamental importance for a final evaluation. In otherwise unremarkable deliveries at term, four conditions must be fulfilled to postulate a causal relationship between asphyxia and the development of cerebral palsy: The asphyxia must be severe. During the early neonatal period, clinical symptoms of moderate to severe hypoxic-ischaemic encephalopathy with functional impairment of other organs must be present. The neurological symptoms must be typical for intrapartal asphyxia. Documentation of diagnostic evaluation to rule out other forms of pathology must be complete (21).     

Centrilobular necrosis after orthotopic liver transplantation: a longitudinal clinicopathologic study in 71 patients

Centrilobular necrosis (CLN) is a histological finding often encountered after orthotopic liver transplantation, but its pathogenesis is still unknown. In this study, the significance of CLN was assessed in a series of 227 consecutive liver transplantations performed between January 1989, and December 1991. Seventy-one patients (30.9%) showed CLN on at least one biopsy result, which were obtained because of an increase of aspartate aminotransferase activity. Their liver specimens were reviewed, and 19 histological features were recorded with particular attention given to lobular changes in acinar zone 3, to features commonly attributed to cellular and ductopenic rejection, and to changes suggestive of ischemia. CLN could first be observed either soon (within 4 days) or late (up to 3 years) after transplantation. Only 23 (32.4%) specimens had centrilobular necrosis affecting more than 75% of acinar zones 3. In 60 cases (84.5%) the lesion was limited to acinar zone 3. An important associated feature was sinusoidal congestion in 73.2% of cases. Fifty-one of 71 patients (71.8%) had histological features of cellular rejection before or at the time of CLN, and 13 of these progressed to ductopenic rejection versus 3 of the 156 patients without CLN (P < .0001). Nine patients had a recurrence of CLN, of whom 2 progressed to ductopenic rejection, a recurrence rate of 16.7% in this series. The survival of patients with CLN is worsened by associated ductopenic portal tracts compared with those without ductopenia (P = .0189-Mantel-Cox). This histological combination, irrespective of the serum bilirubin level, may warrant an early conversion to FK506-based immunosuppression.     

Diffusion and perfusion magnetic resonance imaging of the evolution of hypoxic ischemic encephalopathy in the neonatal rabbit

Hypoxic-ischemic encephalopathy (HIE) can result from neonatal asphyxia, the pathophysiology of which is poorly understood. We studied the acute evolution of this disease, using magnetic resonance imaging in an established animal model. HIE was induced in neonatal rabbits by a combination of common carotid artery (CCA) ligation and hypoxia. Serial diffusion and perfusion-weighted magnetic resonance images were acquired before, during, and after the hypoxic interval. Focal areas of decreased apparent diffusion coefficient (ADC) were detected initially in the cortex ipsilateral to CCA ligation within 62 +/- 48 min from the onset of hypoxia. Subsequently, these areas of decreased ADC spread to the subcortical white matter, basal ganglia (ipsilateral side), and then to the contralateral side. Corresponding perfusion-weighted images showed relative cerebral blood volume deficits which closely matched those regions of ADC change. Our results show that MRI diffusion and perfusion-weighted imaging can detect acute cell swelling post-hypoxia in this HIE model.     

The acute phase response and laboratory testing

A model of sensitization by intraperitoneal lymph node inoculation was developed to test the hypothesis that hyperacute rejection (HAR) could occur in sensitized recipients of vascularized pancreas allografts. Ten pairs of outbred mongrel dogs that were lymphocytotoxic cross-match assay negative were inoculated with homogenized lymph nodes on either three or four occasions at fortnightly intervals before renal transplantation. A renal allograft from the same donor was used to test the HAR response and to further enhance sensitization by rejection of a vascularized organ. Pancreas transplants were performed 2 weeks later, with biopsies of the graft and blood samples taken at 0, 10, 20, and 30 min and then at 30-min intervals until the grafts were no longer viable. All renal and pancreas grafts were rejected in a classical hyperacute pattern. Within 4 min of revascularization of the pancreas, central lobular hemorrhage and vascular congestion appeared, followed by general edema. Histology demonstrated parallel changes of edema, vascular congestion, necrosis, hemorrhage, and leukocytic infiltrate, which all preceded graft infarction. A sharp decline in both arterial and venous white blood cell count and platelets occurred within 10 min of revascularization with initial sequestration and subsequent release of platelets from the graft (P=0.02). In summary, HAR of the allografted pancreas can be observed by the surgeon within minutes of revascularization, with predictable macroscopic and microscopic changes. This study supports the use of routine lymphocytotoxic cross-match tests for all recipients of pancreas transplants and implies that particular care is warranted in regraft pancreas allograft recipients.     

Kayexalate (sodium polystyrene sulphonate) in sorbitol associated with intestinal necrosis in uremic patients

BACKGROUND: Kayexalate (sodium polystyrene sulphonate) in sorbitol is commonly used to treat hyperkalemia in patients with renal insufficiency. Isolated case reports and one recent large series have documented intestinal necrosis following administration of kayexalate in sorbitol. METHODS: Two patients with luminal kayexalate crystals associated with intestinal pathology were first identified in the pathology department, and clinicopathological correlation was carried out. RESULTS: Both patients were seriously ill, had prior cardiac surgery and were in renal failure (uremic). Examination of autopsy and colonic resection showed luminal kayexalate crystals associated with underlying mucosal necrosis, submucosal edema and transmural inflammation. CONCLUSION: Although occurring in complex clinical settings, the pathological findings provide additional evidence that kayexalate in sorbitol may be associated with intestinal necrosis and inflammation in uremic patients and that this may be a clinically and pathologically under-recognized iatrogenic bowel injury.     

Occlusive laryngotracheitis in turkeys following drinking water administration of gentian violet

Acute respiratory signs and increased mortality due to suffocation occurred in a flock of 5-week-old male turkey poults following water administration of gentian violet. Gross lesions of laryngeal edema and occlusion of the tracheal opening with caseous plugs were present. Microscopic lesions in the tracheas consisted of vascular congestion, mucosal degeneration, and necrosis. The condition was reproduced experimentally in turkey poults by giving drinking water containing gentian violet.     

Selection and maintenance of lung donors

Magnetic resonance imaging (MRI) was performed in ten patients with intracranial lymphoma. Seven were pathologically confirmed and three were clinically diagnosed. Nineteen lesions were found among the ten cases. None had acquired immunodeficiency syndrome (AIDS) or had received immunosuppression therapy. Two lesions were in the lateral and third ventricles, and the others were predominantly in the corpus callosum, deep white matter, or central gray matter. Four patients had multiple lesions. All had mild to severe edema. On T1-weighted images, all lesions showed hypointensity. On T2-weighted images, three lesions showed definite hypointensity to gray matter, and the others showed hyperintensity. The contour of all lesions was well demarcated from the surrounding edema. Eight cases were scanned before and after intravenous administration of 0.1 mmol/kg of gadolinium-dimethylene triaminepentaacetic acid (Gd-DTPA), and all exhibited homogeneous enhancement. Three cases showed blurred enhancement margins. Four cases showed hemorrhage, and the frequency of hemorrhage was higher than in previous reports. Pathological examination was performed in seven cases. All showed dense concentric lymphoma cells without necrosis. There was no pathological difference between the hyperintense and hypointense lesions on T2-weighted images.     

Neuroimaging and pathology of the spinal cord in compressive cervical myelopathy

Magnetic resonance imaging (MRI) has enabled us to see the spinal intramedullary pathology as differences in signal intensity. Intramedullary high intensity lesions were observed on T2-weighted MRI in patients with cervical spondylotic myelopathy (20.0%) and ossification of the posterior longitudinal ligament (OPLL) of the cervical spine (25.7%). The frequency of this findings was proportional to the clinical severity of myelopathy and degree of spinal cord compression. The pathophysiological basis of such signal abnormality was presumed to vary from acute edema to chronic myelomalacia. The intramedullary lesion on MRI is considered to be the main site of lesion responsible for the neurological symptom because of a good correlation between the neurological level and high intensity level. We found from nine autopsy cases of OPLL that there are distinct differences in severity and extent of pathological changes between the spinal cord with a boomerang-shaped cross-section and that with a triangular-shaped cross-section. In the boomerang-shaped cases, major pathological changes were restricted to the gray matter and the white matter was relatively well preserved. Secondary wallerian degeneration was restricted to the fasciclus cuneatus the fibers of which were derived from the affected segments. In the cases of a triangular shape, pathological changes were more severe, both white and gray matter were involved. There were severe pathological changes over more than one segment, and both descending degeneration of the lateral pyramidal tracts and ascending degeneration of the posterior column, including the fasciclus gracilis, were observed. In conclusion, it is clinically very important to understand the pathological basis of the compressed spinal cord on neuroimages.     

Reperfusion injury as the mechanism of brain damage after perinatal asphyxia

Upon reperfusion of ischemic tissues, reactive oxygen metabolites are generated and are responsible for much of the organ damage. Experimental studies have revealed two main sources of these metabolites: 1) the oxidation of hypoxanthine to xanthine and on to uric acid by the oxidase form of xanthine oxidoreductase and 2) neutrophils accumulating in ischemic and reperfused tissue. Blocking either source will reduce reperfusion damage in a number of experimental situations. Although xanthine oxidoreductase activity may be unmeasurably low in organs other than liver and intestine, it may be involved in reperfusion injury elsewhere because of its localization in capillary endothelial cells. Time course considerations suggest that substrate accumulation and NADH inhibition of dehydrogenase activity may be more important in the pathogenesis than conversion of xanthine dehydrogenase into the oxidase form. Neutrophil accumulation may be partly due to oxidants in the first place, suggesting a link between the two sources of reactive oxygen metabolites. In the clinical context, many of the sequelae of perinatal asphyxia may be accounted for by reperfusion damage to organs such as brain, kidney, heart, liver, and lungs. During asphyxia, substrates of xanthine oxidase accumulate, upon resuscitation the cosubstrate oxygen is introduced, and evidence for oxidant production and effects has been obtained. In the pathogenesis of brain damage after asphyxia, both microvascular injury and parenchymal cell damage are important. Oxygen metabolites are involved in the former, but in the latter process their role is less clear because ischemia-reperfusion triggers not only oxidant production but many other phenomena, including gene activation, ATP depletion, glutamate accumulation, and increase of intracellular calcium. A severe insult results in cell necrosis, but more moderate asphyxia may cause delayed neuronal death through apoptosis. The time course of the changes in high energy phosphates as well as of selective neuronal death suggest that in the first hours of life there is a "therapeutic window," with future possibilities for prevention of permanent damage.     

Pathomorphology of the skeletal musculature of swine dying during transportation

Pathomorphological studies were conducted into seven different muscles of 50 pigs that had died on transport to slaughterhouses. Established was the following percentual presence of acute disseminated hyaline-plaque degeneration and necrosis of muscle fibres: Group 1 with high frequency of pathological findings: M. biceps femoris, bright portion positively affected in 72 per cent of all cases, dark portion in 68 per cent; M. semimembranosus affected in 64 per cent; M. longissimus dorsi affected in 56 per cent. Group 2 with low to medium frequency of pathological findings: M. Quadriceps femoris affected in 26 per cent; M. semitendinosus, bright portion affected in 26 per cent, dark portion in 16 per cent; M. psoas major affected in 18 per cent. Group 3 without myopathy frequency: M. masseter. The rare occurrence of resorptive myositis (between zero and six per cent of all cases, depending on affected muscles) seems to confirm the young age of that myopathy which usually develops only under transport stress. Hyaline transverse ligaments (supercontractures) were not observed at all in the context of transport deaths (M. longissimus dorsi, M. biceps femoris--bright portion, M. semitendinosus--bright portion, M. masseter) or only in rare cases (M. quadriceps femoris in two per cent of all cases, M. semimembranosus in six per cent, M. semitendinosus--dark portion in six per cent, M. biceps femoris in 18 per cent, M. psoas major in 24 per cent). A comparison with earlier results on the frequency of muscle damage showed that hyaline-plaque degeneration and necrosis of muscle fibres occurred much more often in the context of normal slaughter without any transport and with much graver severity following different modes of transport. These conclusions and results are all relating to pigs which died on transport. The results are discussed, with reference to aetiology and pathogenesis of myopathies in swine caused by stress.     

Experimental and clinical correlation in acute pancreatitis pathogenesis

Pathological aspects in 100 cases of operated A.P. different in severity are not strictly related to aetiological conditions. Clinical observations have suggested some components of pathogenesis: obstruction of bilio-pancreatic inflow in duodenum at the beginning of the attack, bilio-pancreatic reflux on cholangiograms, strong secretory digestive stimulation before attack. Some experimental animals models (dogs) which can mimic pathogenic mechanism (obstruction of pancreatic flow, common bilio-pancreatic duct, closed duodenal loop, acute cholecystitis) have revealed characteristic pathological changes depending on the initiating process. Our conclusion that severity of pathological changes in A.P. are determined by the initiating mechanisms which may differ in some aetiological condition or may be common for different ones.     

Reducing vancomycin use utilizing a computer guideline: results of a randomized controlled trial

Normal development and hypoxic-ischemic changes of glutamate-aspartate transporters (GLAST) and excitatory amino acid transporter type 4 (EAAT4) were demonstrated in the human cerebellum. GLAST-immunoreactive Bergmann's glia and EAAT4-positive Purkinje cells showed a specific distribution and localization, and developed with age in the molecular and Purkinje cell layers. The dendrites and cell bodies of Purkinje cells, which showed EAAT4 immunoreactivity, were ensheathed by GLAST processes. In neonatal hypoxic-ischemic encephalopathy (HIE), GLAST immunoreactivity decreased in the molecular layer and increased in the inner granule cell layer at an early stage, and markedly increased in the Purkinje and inner granule cell layers at a late stage. EAAT4 immunoreactivity decreased with post-ischemic changes of Purkinje cells. GLAST reactivity changed more rapidly than EAAT4 in cases of HIE. These changes of GLAST and EAAT4 may be closely related to the vulnerability of Purkinje cells in hypoxia-ischemia. The glutamate transporter of Bergmann glia may play a more important role in the regulation of the extracellular glutamate concentration in hypoxia and/or ischemia.     

Airway lesions and superoxide dismutase (SOD) distribution in bronchopulmonary dysplasia (BPD)

We examined 71 cases of bronchopulmonary dysplasia (BPD) at autopsy and divided them into five groups on the basis of the patients' survival time, studying on the histological changes in the airways for the purpose of clarifying the pathogenesis of BPD from hyaline membrane disease (HMD). Furthermore, bronchiolar occlusion was classified into four types: secretion, obliterative bronchiolitis, intraluminal plug, and hyperplasia of bronchiolar components. The same occlusive findings as in bronchioli and hyaline membrane were observed from respiratory bronchioles to alveolar ducts. However, there was no obvious correlation between airway lesions and accompanying alveolar lesions excepts three cases of obliterative bronchiolitis. Furthermore, immunohistochemical studies with anti-human SOD antibodies were performed. Mn-SOD was positive for alveolar macrophages in longer surviving infants without significant correlation with histological variation, whereas slightly positive or negative in infants who died within 1 week; CuZn-SOD was rarely positive in any cases. These results is highly correlated to the pathogenesis of BPD and to its pathological advancement with its clinical course.     

Electrophysiological studies in the follow-up of children with perinatal asphyxia history

OBJECTIVES: The objective of this study was to analyze the usefulness of electrophysiological studies [electroencephalogram (EEG) and auditory-evoked potential (AEP)] during the follow-up of children with perinatal asphyxia antecedents. PATIENTS AND METHODS: A prospective epidemiological study of perinatal asphyxia in term neonates born at the University Hospital San Juan (Alicante, Spain) between November 1991 and February 1995 was performed. Perinatal asphyxia was graded as non-severe (1 minute Apgar score < or = 6 and/or umbilical artery pH < 7.20, with abnormal fetal heart patterns and/or meconium-stained amniotic fluid and the need for immediate neonatal resuscitation) and severe (1 minute Apgar score < or = 3 and umbilical artery pH < 7.10). The incidence of hypoxic-ischemic encephalopathy (classification of Levene and Sarnat & Sarnat) during the neonatal period and neurological sequelae (classification of Finer and Amiel-Tison) during the follow-up period were studied. Electrophysiological studies (EEG and AEP) were made mainly between 12 and 18 months of life. RESULTS: During the study period there were 156 cases of perinatal asphyxia in full-term live births (31 severe and 125 non-severe). Hypoxic-ischemic encephalopathy was present in 25.6% of asphyxiated newborn infants, being mild in 30 cases, moderate in 5 and severe in 5. The incidence of neurological sequelae in 115 asphyxiated newborns followed for 24 month was 16.5%. This included mainly motor disabilities. We did not find any case of epilepsy, but there were 4 children with febrile seizures and one case of benign myoclonic seizures. EEG was performed in 88 cases during follow-up, and only was abnormal in two infants without seizures. AEP was performed in 82 cases during follow-up and hearing loss was detected in 4 children with neurosensorial hypoacusia (3 unilateral and 1 bilateral). CONCLUSIONS: Rutinary EEG is not useful during follow-up of children with antecedents of perinatal asphyxia. However, AEP is a hearing screening procedure for infants at risk of deafness, such as in perinatal asphyxia, and the cases of neurosensorial hearing loss detected by AEP in our population were clinically unapparent.     

Sodium metabisulfite and SO2 release: an under-recognized hazard among shrimp fishermen

Since the introduction of sodium metabisulfite as a food preservative, it has been associated with several idiosyncratic reactions (eg, bronchospasm, oculonasal symptoms, and urticaria/angioedema) in sulfite-sensitive individuals. The pathogenic mechanism of these reactions is not yet understood. We report the case of two crewmen on a shrimp trawler who were found dead in the ship's hold. Their deaths had occurred while they were applying dry sodium metabisulfite, referred to as "shrimp dip" in the shrimping industry. Postmortem examinations showed diffuse pulmonary edema consistent with death secondary to asphyxia. Associated findings were visceral congestion. Although it is possible to measure death from sodium metabisulfite with available records, its potential morbidity cannot be estimated. It is known that sodium metabisulfite can react with acids and water, releasing toxic sulfur dioxide (SO2) gas. In addition, SO2 gas reacts with respiratory tissue forming sulfureous acid, and inducing a pulmonary reaction causing hypoxemia. Furthermore, sodium metabisulfite, compared with sodium bisulfite, has a much greater propensity to release SO2 gas. We conclude that there is a need for improved education regarding the potential side effects of sodium metabisulfite, thus eliminating needless occupational morbidity and mortality.     

The roles of muscarinic receptor subtypes in modulation of nasal ciliary action

OBJECTIVE: Clinicopathological features of mycobacteriosis were studied by means of microscopical examination of 34 autopsy cases in patients with acquired immunodeficiency syndrome (AIDS) and the diagnostic methods were evaluated. METHODS: All cases were anatomized, sampled, fixed and embedded routinely and stained with hematoxylin-eosin. Acid fast stain was applied to identify the mycobacteria. The pathological sections and files were reviewed systemically and retrospectively. RESULTS: Thirty-four cases of mycobacteriosis, including Mycobacterium avium-intracellular complex (MAI) infection (20 cases) and Mycobacterium tuberculosis (10 cases) and mixed infection of both pathogens (4 cases) were found out of 151 autopsy AIDS patients. MAI infection involved mostly the lymph nodes (21 cases) and followed by spleen, liver and lung, etc. The infection were often disseminated and characterized by proliferation of histocytes with foamy or vacuolar cytoplasm containing acid fast bacilli and formation of granulomatous nodules. Tuberculosis often involved the lung (10 cases) and lymph node (8 cases), the typical manifestations of which were caseous necrosis and tuberculation. Other opportunistic infections and neoplasmas occurred with mycobacteriosis in 25 cases. CONCLUSIONS: Mycobacteriosis, especially the tuberculosis and MAI infection are common in patients with AIDS, which are often disseminated and involved the lung and lymph node. The diagnosis can be made according to the specific pathological appearances and positive acid fast stain.     

Oxyntomodulin: a cAMP-dependent stimulus of rat parietal cell function via the receptor for glucagon-like peptide-1 (7-36)NH2

Six patients with hepatocellular carcinoma were subjected to percutaneous microwave coagulation therapy (PMCT) by ultrasonic guiding. The size of the main tumor in the present cases was limited to not more than 2 cm. From 18 to 48 days after PMCT, each patient was subjected to surgery and pathological examination. By macroscopic observation, the PMCT area including both non-tumor and tumor regions looked yellowish white, and the boundary was clearly recognized. In the histological examination, the coagulation area surrounded by fibrous capsule was found, and deletion of nuclei and changes in stainability were observed in the marginal region. These changes indicated obvious coagulation necrosis, but the changes became less intense toward the center in the area, and in some portions, the tissue was indistinguishable from viable cells by light microscopy. In 2 cases out of the 6, part of the tumor remained outside the coagulation area. Since only the area determined by the microwave electrode is coagulated to cause necrosis on PMCT, sufficient safety margin should be required.