Persistent Depression of the Lambda Site with Progressive Skull Deformity May Be a Sign of Suture Closure: Case Series and Pathologic Consideration.

BACKGROUND: Flat head syndrome (FHS) sometimes occurs when a baby maintains the same head position during the first several months of life, causing a skull deformity. FHS usually improves with time and natural growth, although some show aggravation against conservative treatment. We reviewed pathologically proved early closure of skull suture that may be seen secondary to FHS. METHODS: The clinical and radiologic findings of the patients who showed progressive skull deformity resembling FHS were retrospectively reviewed. All the patients underwent surgical treatment and pathologic specimens were obtained. RESULTS: The detected patients included two 5-month-old infants and one 1-year-old child. The former were conservatively treated without any obvious premature suture closure on computed tomography (CT), and later developed progressive tower-like skull deformities. The infants were diagnosed with possible premature fusion of lambda site and underwent removal around lambda depression (LD). The latter showed evident sagittal suture closure on CT with digital markings, and was diagnosed with increased intracranial pressure and underwent cranioplasty of posterior expansion. Histopathologic specimens obtained from the patients' resected sutures showed irregularly narrowed suture structure with ossification and fibrous tissue proliferation within them, supporting the diagnosis of premature closure of the sagittal sutures. Their postoperative courses were uneventful, and their skull deformities subsequently improved. CONCLUSIONS: Conservative therapy-resistant progressive occipital skull deformity with LD may be a sign of early suture closure, even if CT does not show obvious suture closure. The findings are helpful for early diagnosis and might lead to minimal invasive surgery if needed.

Impaired Consciousness in a Coronavirus Disease 2019 Patient Caused by Low Serum Sodium: A Case Report.

A 30 year-old man with a high fever (37.5°C-40°C), vomiting, slurred speech, and mild cognitive impairment was admitted to our Emergency Department. He had traveled from Spain to the UK on business at the end of February 2020. A nasopharyngeal swab was positive by RT-PCR for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), but a cerebrospinal fluid (CSF) sample was negative. His neurological abnormalities recovered completely on saline infusion to normalize his low serum sodium level. Although neurological abnormalities in patients with COVID-19 are rare, it is important to distinguish the etiologies including encephalitis, meningitis, or merely electrolyte abnormalities.

Fatal adult case of severe lymphocytopenia associated with reactivation of human herpesvirus 6.

It has been suggested that immunosuppression associated with human herpesvirus 6 (HHV-6) infection is a result of functional impairment or direct destruction of immunological cells. The ability of the virus to infect and destroy lymphocytes may cause progressive immunodeficiency in an infant with primary HHV-6 infection. An adult patient is described who had a fatal cytomegalovirus (CMV) infection due to severe and prolonged lymphocyte depletion associated with HHV-6 reactivation. The HHV-6 antibody titers were increased significantly after reactivation, and the virus was isolated from his peripheral blood mononuclear cells. The quantity of both HHV-6 and CMV DNA was determined by using real-time PCR in plasma samples collected serially. HHV-6 DNAemia persisted for 1 month, which started just 1 week after the onset of lymphocytopenia. In contrast to HHV-6, CMV DNAemia was detected in the terminal phase of the illness. Thus, HHV-6 reactivation may have been the cause of the severe lymphocyte depletion and fatal CMV infection.

Multiple perforated ulcers of the small intestine associated with allergic granulomatous angiitis: report of a case.

Although allergic granulomatous angiitis (AGA) is occasionally associated with gastrointestinal lesions, multiple perforated ulcers of the gastrointestinal tract are uncommon. We report herein a case of AGA associated with multiple perforated ulcers that erupted in the small intestine during corticosteroid therapy. A 31-year-old Japanese man was admitted to our hospital with epigastralgia, edema of the bilateral lower extremities, and general malaise. He had a persistent high fever, abdominal pain, and watery diarrhea. Laboratory data showed remarkable eosinophilia. The abdominal pain became exacerbated after the administration of oral prednisolone. Physical examination indicated positive signs of peritoneal irritation in the entire abdomen, and abdominal computed tomography scanning showed intra-abdominal free air, suggesting generalized peritonitis due to intestinal perforation. Laparotomy revealed multiple perforated ulcers in the jejunum and ileum. Histological examination indicated remarkable eosinophilic infiltration in the surrounding area of the small arteries and arterioles located in the submucosal layer, which was compatible with AGA. Although the association of intestinal perforation with AGA is relatively infrequent, intensive perioperative management is essential to ensure a favorable clinical outcome, particularly during the period on corticosteroid therapy.