A case of community-acquired Clostridioides difficile infection causing intussusception, severe pneumonia, and severe hypokalemia.

BACKGROUND: Clostridioides difficile infection is associated with antibiotic use and manifests as diarrhea; however, emerging cases of fulminant diarrhea caused by binary toxin-producing C. difficile unrelated to prior antibiotic exposure have been reported. Although fulminant colitis caused by C. difficile has been documented, instances of intussusception remain scarce. Here, we present a case of adult intussusception with severe hypokalemia and pneumonia resulting from a community-acquired C. difficile infection in Japan. CASE PRESENTATION: An 82-year-old male presented with dizziness, progressive weakness, and diarrhea. Initial vital signs indicated severe respiratory and circulatory distress, and laboratory findings revealed hypokalemia, pneumonia, and septic shock. Imaging confirmed intussusception of the ascending colon. Although colonoscopy suggested a potential tumor, no malignancy was found. The C. difficile rapid test result was positive, indicating community-acquired C. difficile infection. Treatment with vancomycin was initiated; however, intussusception relapsed. Surgical intervention was successful and led to clinical improvement. The patient's complex pathophysiology involved community-acquired C. difficile-induced severe diarrhea, hypokalemia, hypermetabolic alkalosis, and subsequent intussusception. Although adult intussusception is uncommon, this case was uniquely linked to binary toxin-producing C. difficile. The identified strain, SUH1, belonged to a novel sequence type (ST1105) and clade 3, suggesting a highly virulent clone. Resistome analysis aligned with phenotypic susceptibility to metronidazole and vancomycin, confirming their treatment efficacy. CONCLUSION: This case report highlights a binary toxin-producing C. difficile that caused intussusception. The consideration of community-acquired C. difficile in the differential diagnosis of severe enteritis is necessary, even in Japan.

Prompt diagnosis and appropriate treatment of Japanese spotted fever: A report of three cases.

Background: Japanese Spotted Fever (JSF) is a Spotted Fever Group (SFG) rickettsiosis caused by Rickettsia japonica. More than 300 cases are diagnosed annually in Japan, and the number of reported cases has been increasing. Correct diagnoses depend on the triad of symptoms and signs, including fever, rash, and eschar, which can be seen at the site of vector bites. JSF is not life-threatening if treated appropriately without diagnostic delay but there are some fatal cases every year. This negligence leads to disseminated intravascular coagulation (DIC) and multiple organ failure (MOF), and poor prognoses, consequently. Prompt diagnosis of JSF is difficult when the aforementioned triad of signs and symptoms is not initially present. Case report: This report describes three JSF cases: an 87-year-old woman with fever, shock, pancytopenia, DIC, and MOF; a 79-year-old man with fever and difficulty in movement; and a 78-year-old man with fever, general fatigue, and appetite loss. All patients had a rash and eschar, which led to prompt diagnosis and appropriate treatment immediately. All patients were treated without any complications. Why should an emergency physician be aware of this?: As mentioned above, JFS can be fatal with delayed diagnoses and treatment initiations. The key for a prompt diagnosis is to recognize the triad of symptoms and signs, which are not often present initially, and it makes JSF diagnosis challenging. Repeated comprehensive physical examinations are essential for prompt diagnosis and improve prognosis of JSF.

[Full Recovery from Cardiopulmonary Arrest caused by Traumatic Asphyxia].

Traumatic asphyxia is a crush injury of the chest characterized by facial edema, cyanosis, conjunctival hemorrhage, and petechiae on the face and chest. The prognosis depends on the duration of chest compression and early cardiopulmonary resuscitation after cardiopulmonary arrest. Here we report a case of full recovery from cardiopulmonary arrest caused by traumatic asphyxia. The chest of a 56-year-old man was compressed by a machine while working. Immediately, his colleague started cardiopulmonary resuscitation, which was successful. When he was admitted to our hospital, his consciousness level was E1V2M2(Glasgow coma scale). Our treatment included therapeutic hypothermia, the duration of which was 24 hours at 34 °C. Rewarming his body to 36 °C took place over 48 hours. Thereafter, he recovered completely and was discharged on the 12th hospital day without neurologic sequela. Therapeutic hypothermia was possibly effective in this case.

Left atrial remodeling and recurrence of congestive heart failure in patients initially diagnosed with heart failure.

BACKGROUND: Left atrial volumes (LAVs) have been suggested to represent long-term exposure to elevated pressures. This study examined the recurrence of heart failure (HF) based on LAV in patients initially diagnosed with congestive HF (CHF). METHODS: This study comprised 77 patients (age, 75 ± 8 years) with well-documented, clinically defined HF, and complete two-dimensional echocardiographic examinations. The echocardiographic examinations were performed on admission and after medical treatment (90 ± 43 days after initial examination). Patients with atrial fibrillation, flail mitral valve, or mitral valve replacement were excluded from this study. RESULTS: The initial left ventricular ejection fraction (LVEF) was 44 ± 17% and the indexed LAV (LAVI) was 61 ± 22 mL/m(2) . After medical treatment, a decreased LAVI was observed in 38 patients and an increased LAVI (LA remodeling) was observed in 39 patients. With median follow-up periods of 454 days, compared to patients with decreased LAVI, patients with LA remodeling had a significantly higher incidence of CHF recurrence (P = 0.008). Patients with LA remodeling had a CHF-free survival rate of 36 ± 13% vs. 81 ± 9% (those without LA remodeling). A multivariate analysis indicated that, follow-up LV end-systolic volume (P = 0.04), LVEF (P = 0.005) and LAVI (P = 0.04) independently predicted CHF recurrence. CONCLUSIONS: Patients initially diagnosed with CHF follow divergent courses based on their LAV. LA remodeling after medical treatment can be useful for predicting CHF recurrence during follow-up.

Novel method for quantitative evaluation of cardiac amyloidosis using (201)TlCl and (99m)Tc-PYP SPECT.

OBJECTIVE: The degree of myocardial technetium-(99m)-pyrophosphate ((99m)Tc-PYP) accumulation in cardiac amyloidosis is conventionally evaluated by the PYP score. This method involves qualitative visual evaluation on two-dimensional images. Here, we performed three-dimensional quantitative analysis using software developed in our laboratory. METHODS: We performed dual myocardial imaging using thallium-(201)-chloride ((201)Tl-Cl) and (99m)Tc-PYP in cases of suspected cardiac amyloidosis and calculated the PYP accumulation rates of all myocardial pixels showing (99m)Tc-PYP accumulation. We defined this procedure as quantitative evaluation of the degree of (99m)Tc-PYP accumulation in the myocardium. Patients were divided into two groups with and without a diagnosis of cardiac amyloidosis, and we examined the PYP accumulation rates in both groups. In addition, we examined the PYP scores of the two groups by conventional qualitative evaluation. RESULTS: The PYP scores of the cardiac amyloidosis group were significantly higher than those of the other group. The PYP accumulation rates of the cardiac amyloidosis group were significantly higher than those of the other group. There were significant differences in the PYP accumulation rate and PYP score between the two groups. There was considered to be a threshold between the two groups in the case of the PYP accumulation rate. CONCLUSIONS: When the threshold of the PYP score was defined as 3+ and that of the PYP accumulation rate as 41.5 %, the sensitivity of the PYP score and PYP accumulation rate was 84.6 %. However, the specificity of the PYP accumulation rate was higher than that of the PYP score. Quantitative evaluation by the PYP accumulation rate of the degree of (99m)Tc-PYP accumulation in the myocardium may be useful in the diagnosis of cardiac amyloidosis.

Factors influencing left atrial volume in treated hypertension.

BACKGROUND: Left atrial (LA) enlargement has been documented to occur in hypertension (HT), and has been an index for evaluating the diastolic function of the left ventricle. Enlargement of the LA is one of the vital factors that induce heart failure and atrial fibrillation (AF) in patients with HT. METHODS AND SUBJECTS: 130 treated hypertensive patients were enrolled. All recruits participated in an echocardiogram, electrocardiogram, a routine blood examination including brain natriuretic peptide (BNP), and physical examinations. RESULTS: Left ventricular mass (LVM) indexed to height(2.7) had a significant positive correlation with left atrial volume index (LAVI) (p<0.0001), as well as natural logarithm BNP (p<0.001). Blood pressure levels were not associated with LAVI, neither body mass index nor age. LAVI had a positive correlation with factors involving the left ventricle volume, LVM, and right ventricle systolic pressure (RVSP) (r=0.687, p<0.0001). The parameters of LV diastolic function were positively but weakly associated with LA size. In the subgroup of LAVI, the evidence of paroxysmal atrial fibrillation (PAF): LAVI<32 ml/m(2) had no PAF, whereas the incidence of PAF was 7.5%, 11.4%, and 15.2%, respectively in the LAVI>32 ml/m(2) group. Of anti-hypertension drugs, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers had a tendency to reduce LAVI; however, there was no statistical significance within the groups. CONCLUSIONS: Left ventricular volume and mass are independent factors affecting LAVI in treated HT. The incidence of PAF is associated with LA size. In patients with treated HT, LA size may be a useful surrogate marker for monitoring the effectiveness of medical therapy and occurrence of AF.

A case of long QT syndrome having compound mutations of KCNH2 and SCN5A.

Long QT syndrome (LQTS) is a hereditary ion channelopathy resulting in prolonged cardiac repolarization and abnormal prolongation of the QT interval on the electrocardiogram (ECG). The patients are likely to develop ventricular arrhythmias and sudden cardiac death. Molecular biology and basic electrophysiology studies revealed an approach to the management of patients with LQTS, which includes genotype-based risk stratification. A 16-year-old-woman with QT prolongation on ECG had frequent syncopal episodes and an attack of ventricular tachycardia followed by ventricular fibrillation. The SCN5A mutation (intravene sequence 4-1 c/t) in addition to the KCNH2 mutation (Arg56Gln) was identified. Her mother and older sister were also diagnosed as having LQTS, but had only a single mutation (KCNH2). Her older sister had an episode of syncope, but her mother did not. Genetic analysis sometimes reveals 2 or more mutations in LQTS patients with clinical phenotypes of the Romano-Ward syndrome. Compound mutations in different LQTS-related genes are likely to modify clinical characteristics. In addition, comprehensive screening of LQTS-related genes might be needed when facing family members with different clinical manifestations. .

Activation of inducible NOS in peripheral vessels and outcomes in heart failure patients.

BACKGROUND: Activation of inducible nitric oxide synthase (iNOS) has been reported in congestive heart failure (CHF) conditions. However, it is unknown whether activation of iNOS affects prognosis of CHF patients. We prospectively studied the influence of activation of iNOS in the forearm on the outcome of CHF patients. METHODS AND RESULTS: Forearm blood flow (FBF) responses to 3 doses of acetylcholine (ACh) and nitroglycerin (NTG), and 4 doses of a selective iNOS inhibitor (aminoguanidine: Amn) and a nonselective NOS inhibitor (L-NMMA) were examined using plethysmography in 68 patients with CHF from idiopathic dilated cardiomyopathy. Plasma brain natriuretic peptide (BNP) and tumor necrosis factor-alpha (TNF-alpha) were also measured in all patients. During the mean follow-up period of 3.8 years, 25 patients were hospitalized for worsening heart failure and 9 of these patients died. Patients with adverse events had a diminished vasodilator response to ACh (P < .001) compared to patients without adverse events. Amn significantly decreased FBF (P < .001) in patients with adverse events, but not in patients without adverse events. FBF responses to NTG and L-NMMA were not significantly different between the 2 groups. When grouped by maximum FBF responses to each drug above and below the median value, multivariate Cox proportional hazards model analyses for cardiac event showed a significance in the FBF response to Amn (adjusted hazard ratio 5.89, P < .001). FBF responses to maximum dose of Amn significantly correlated with BNP and TNF-alpha levels (both P < .001). CONCLUSIONS: CHF patients with vascular iNOS activation, as demonstrated by a greater vasoconstrictor response to Amn, had poor outcomes. Activation of iNOS in peripheral vessels, associated with proinflammatory cytokines in accordance to the severity of heart failure, is a marker for, or contributes to, adverse events in patients with CHF.

Nitric oxide-mediated vasodilatory effect of atrial natriuretic peptide in forearm vessels of healthy humans.

1. The aim of the present study was to determine whether the vasorelaxant effect of atrial natriuretic peptide (ANP) is, in part, endothelium dependent in humans. 2. We used veno-occlusive plethysmography to measure forearm blood flow (FBF) during intra-arterial infusions of ANP (4, 8, 16, 32 pmol/min per dL forearm tissue volume) before and after the inhibition of nitric oxide (NO) synthesis by N(G)-monomethyl-L-arginine (L-NMMA; 100 micromol) in seven normal healthy subjects. 3. Atrial natriuretic peptide caused a dose-dependent increase in FBF both before and after L-NMMA and significantly reduced the plasma concentration of angiotensin (Ang) II. Administration of L-NMMA significantly diminished the increase in FBF in response to ANP infusion (P < 0.05). 4. These results suggest that the forearm vasodilative response to ANP is modulated, in part, by an endothelium-derived NO-mediated mechanism associated with a decrease in AngII caused by ANP.