Neuroleptic malignant syndrome (NMS) is a rare life-threatening condition associated with the use of antipsychotic medications. This case report describes a male patient in his early 30s who presented with fever, breathlessness, and lower limb weakness, ultimately diagnosed with NMS despite the absence of muscular rigidity. On examination, he was febrile, tachycardic, and tachypneic with an oxygen saturation of 88% and elevated blood pressure. On auscultation diffuse crepitations in both lungs were revealed. Neurological assessment indicated motor strength of 3/5 in both lower limbs, without rigidity, sensory loss, or cerebellar signs. It was noted that he was on irregular atypical antipsychotic medication for the past one year. Laboratory investigations revealed leukocytosis, elevated transaminases, dyselectrolytemia, elevated creatine phosphokinase (CPK), and serum creatinine. NMS was not initially considered due to the lack of muscular rigidity. However, the patient later developed autonomic dysregulation manifestations, such as paralytic ileus. Once organic causes were excluded, NMS was diagnosed. Supportive therapy included 23 cycles of hemodialysis and colonic decompression for pseudo-obstruction. He was treated with intravenous fluids and dopamine receptor agonist medications. NMS usually presents with fever, muscular rigidity, altered mental status, and autonomic instability; yet, the absence of muscular rigidity in this patient is a distinctive and unusual feature.

Still\'s disease is frequently a condition of exclusion for patients with an unidentified cause of fever. Accompanying symptoms typically include fever, arthralgia, and a transient skin rash. The underlying pathophysiology indicates an autoimmune origin. Diagnosis is primarily clinical, often utilizing the Yamaguchi criteria. The case in question involves a 19-year-old male presenting with high-grade fever and paralytic ileus. The patient received intravenous glucocorticoids and cyclophosphamide, resulting in a rapid clinical improvement. During the follow-up, tofacitinib was initiated based on the clinical response observed.

This case report examines the possible correlation between the clozapine/norclozapine ratio and the occurrence of constipation and paralytic ileus. We present the case of a 42-year-old patient diagnosed with schizoaffective disorder undergoing clozapine therapy. Despite intensive treatment with clozapine, haloperidol, valproic acid and biweekly electroconvulsive therapy sessions for over a year, florid psychotic symptoms and fluctuating mood swings persisted. Therefore, valproic acid was replaced by carbamazepine, a potent inducer of several CYP450-enzymes. To maintain clozapine plasma levels, fluvoxamine, a CYP1A2-inhibitor, was introduced at a dose of 25 mg before this switch. After addition of carbamazepine, there was a significant decline in clozapine levels, necessitating an increase in fluvoxamine dosage to 50 mg. Five weeks later the patient was admitted to a general hospital with a diagnosis of paralytic ileus. Treatment with enemas proved effective. Drug concentration analysis revealed a 2.5-fold increase in norclozapine levels in the weeks preceding hospital admission, resulting in an inverted clozapine/norclozapine ratio. Treatment with clozapine, carbamazepine and fluvoxamine was continued as the patient demonstrated clinical improvement on carbamazepine. Concurrently, an intensive laxative regimen was initiated. Two weeks later, the patient was readmitted to the general hospital due to suspected paralytic ileus and faecal vomiting, once again displaying an inverted clozapine/norclozapine ratio. We discuss potential mechanisms contributing to the occurrence of the paralytic ileus in this patient, including the antagonism of muscarinic M3 receptors by both clozapine and norclozapine, as well as the agonism of delta-opioid receptors by norclozapine. This case highlights the potential significance of both the clozapine/norclozapine ratio and absolute norclozapine levels as risk factors for constipation and paralytic ileus in patients on clozapine therapy.

Patients with systemic autoimmune rheumatic diseases are at a high risk for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and effective antiviral treatments including nirmatrelvir/ritonavir can improve their outcomes. However, there might be potential drug-drug interactions when these patients take nirmatrelvir/ritonavir together with immunosuppressants with a narrow therapeutic window, such as tacrolimus and cyclosporine. We present a case of paralytic ileus resulting from tacrolimus toxicity mediated by the use of nirmatrelvir/ritonavir in a patient with systemic lupus erythematosus (SLE). A 37-year-old female SLE patient was prescribed nirmatrelvir/ritonavir without discontinuing tacrolimus. She presented to the emergency room with symptoms of paralytic ileus including persistent abdominal pain, nausea, and vomiting, which were verified to be associated with tacrolimus toxicity. The blood concentration of tacrolimus was measured >30 ng/mL. Urgent medical intervention was initiated, while tacrolimus was withheld. The residual concentration was brought within the appropriate range and tacrolimus was resumed 8 days later. Physicians must be aware of the potential DDIs when prescribing nirmatrelvir/ritonavir, especially to those taking immunosuppresants like tacrolimus.

Hepatic portal venous gas (HPVG) is an infrequent and life-threatening condition with high morbidity and mortality rates, which consists of the presence of gas in the portal vein and its branches. Improvements in imaging technologies have led to the diagnosis of HPVG in less severe circumstances, which, in turn, has only determined a small amelioration of the prognosis. We present a rare case of HPVG subsequent to paralytic ileus in a patient who attained long-term survival after the surgical treatment was performed. HPVG is considered to be associated with sepsis, parietal/mucosal damage, inflammation of the intraperitoneal organs, and meteorism, which may be found in a variety of pathologies. The severity of this pathology depends on the pre-existing conditions of the patients but also on how quickly a treatment plan is established and applied. As a correct and timely diagnosis is crucial for the increase of the survival rate in HPVG, greater attention shall be paid to the clinical manifestations and the differential diagnosis.

暂无摘要。

Malaria is a life-threatening, parasitic disease that continues to infect millions of people, especially in endemic regions. Despite advancements in malaria treatment, treating the disease remains challenging. One major challenge is identifying the disease from its unconventional manifestations. Therefore, recognizing its unusual clinical presentations is imperative in early detection and management with a better prognosis. This case report highlights the unique finding of paralytic ileus from a patient with confirmed malaria. Further investigation on the concurrence between paralytic ileus and malaria may aid in identifying the disease and subsequent improvement in treatment.

Bromadiolone, commonly known as super warfarin, is a long-acting coumarin dicoumarin rodenticide. The mechanism of bromadiolone is mainly to inhibit vitamin K1 epoxide reductase and affect the synthesis of coagulation factors Ⅱ, Ⅶ, Ⅸ and Ⅹ, which causes blood coagulation dysfunction and systemic multiple organ hemorrhage. Here, we report of a case of bromadiolone poisoning patient who had digestive tract, abdominal hemorrhage, as well as secondary paralytic ileus. After blood product transfusion and vitamin K1 supplementation, the patient was discharged after the physical condition was improved. It\'s suggestied that clinicians should pay attention to rare complications to prevent missed diagnosis when treating other bromadiolone poisoning.
溴敌隆是一种长效香豆素类抗凝类杀鼠剂，俗称\"超级华法林\"，其作用机制主要是抑制维生素K1环氧化物还原酶，影响凝血因子Ⅱ、Ⅶ、Ⅸ和Ⅹ的合成，致使机体凝血机能障碍，导致全身多脏器出血。本文报道一例溴敌隆中毒后导致消化道、腹腔出血，同时继发麻痹性肠梗阻的患者，给予输注血制品、补充维生素K1等治疗后，病情好转出院。提示临床医生在救治其他溴敌隆中毒时，要注意少见并发症，以免漏诊。.

BACKGROUND: Benzyl alcohol is used as stripping agent in paints and other applications, and benzyl alcohol poisoning is indicated by symptoms, such as impaired consciousness, respiratory depression, hypotension, metabolic acidosis, and renal dysfunction.
METHODS: A 27-year-old Asian man was transported to a hospital for severe disturbance of consciousness following exposure to a paint stripper containing benzyl alcohol, ethylene glycol, and hydrogen peroxide, which he was using to repaint a bridge. The patient was treated under sedation for benzyl alcohol poisoning. On day 3 of hospitalization, his abdominal computed tomography scan revealed a paralytic ileus, so he was transferred to our hospital. The combined toxicity from multiple substances, mainly benzyl alcohol, was thought to be a contributing factor for the paralytic ileus. Upon arrival, the patient also had chemical burns, hypernatremia, and elevated myogenic enzyme levels. His urinary hippuric acid level was high (14.9 g/L) upon admission to the previous hospital. We treated the patient with artificial respiration management, while avoiding high-density oxygen, and with gastrointestinal decompression by gastric tube implantation; laxatives were also administered. The paralytic ileus improved on the 4th day, the tube was removed on the 6th day, and the patient was discharged on the 11th day of hospitalization. No apparent complications were observed at discharge.
CONCLUSIONS: To the best of our knowledge, this is the first case report of paralytic ileus caused by benzyl alcohol, although multiple factors may have influenced the symptoms. After exposure to benzyl alcohol by inhalation and dermal absorption, the patient developed impaired consciousness, metabolic acidosis, and paralytic ileus, and the presence of elevated urinary hippuric acid led to a definitive diagnosis.

Narcotic bowel syndrome is defined as worsening abdominal bloating and cramping with chronic opiate use, leading to paralytic ileus. This syndrome is common yet underreported in adults. However, there is no current evidence of such conditions in the newborn after exposure in utero to high doses of opiates. Our patient was a female indigenous preterm infant born to a mother on a high dose of methadone. On admission at the age of 12 h, she was found to have significant gastric distension. Initial abdominal X-ray showed a large gastric bubble with little evidence of rectal gas. Malrotation was suspected and surgical intervention was discussed. However, repeat abdominal X-ray, ultrasound and upper Gastrointestinal series were found to be normal and without acute findings. Thus, surgery was avoided. The gastric distension resolved spontaneously. She never required opiate therapy for neonatal abstinence syndrome. Given the pattern of gas seen on the initial abdominal X-ray and its spontaneous resolution after removal of maternal methadone, we suspect this baby had neonatal narcotic bowel syndrome. This has never been reported in the literature and is a unique finding. Given the lack of current reports, further observations for this syndrome should be conducted.