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Pulmonary edema of enterovirus 71 encephalomyelitis is associated with left ventricular failure: implications for treatment

Fu YC, Chi CS, Jan SL, Wang TM, Chen PY, Chang Y, et al.

Pediatr Pulmonol, 2003 Apr;35(4):263-8.
PMID: 12629622

Epidemics of enterovirus 71 infections caused the rapid death of many children in Malaysia in 1997 and in Taiwan in 1998. Pulmonary edema occurred in most of the fatal cases and was considered to be neurogenic. The role of the heart was rarely investigated before. Between January 1998-January 2001, 34 consecutive patients who were admitted to the intensive care unit due to enterovirus infection were studied prospectively. Patients were divided into two groups: group I with pulmonary edema, and group II without pulmonary edema. Comparisons were made between the two groups based upon demographic, neurological, and cardiovascular manifestations. Group I consisted of 11 patients (5 boys, 6 girls; mean age, 22.8 months), and group II of 23 patients (12 boys, 11 girls; mean age, 28.8 months). There were no significant differences between the two groups in comparing sex, age, body weight, neurological severity, intracranial pressure, cell count, protein and glucose levels in cerebral spinal fluid, and blood pressure. All group I patients had left ventricular dysfunction, and their ejection fractions were significantly lower than those of patients in group II (37 +/- 11% vs. 75 +/- 6%, P < 0.001). Group I heart rates were higher than those of group II (175 +/- 24 vs. 137 +/- 25, P < 0.001). In group I, 9 patients who received conventional treatment died, and the only two survivors received left ventricular assist devices. In conclusion, the pulmonary edema of fulminant enterovirus 71 infection is associated with left ventricular failure. Left ventricular function is the major determinant of outcome. Early recognition of heart failure and aggressive cardiac intervention are life-saving. Pediatr Pulmonol. 2003; 35:263-268.

Matched MeSH terms: Pulmonary Edema/therapy
Salvaging "hopeless" post head injury patients

Delikan AE, Namazie M

Med J Malaysia, 1979 Sep;34(1):42-5.
PMID: 542150
Matched MeSH terms: Brain Edema/therapy
Multiple subcutaneous puncture and stoma bag drainage for gross lower limb edema: a case report

Beng TS, Chin LE

J Palliat Med, 2010 Aug;13(8):1037-8.
PMID: 20712471 DOI: 10.1089/jpm.2009.0314

We present a case of gross lower limb edema in a 21-year-old man with an intra-abdominal malignant fibrous histiocytoma. He had a 1-month history of lower limb edema secondary to inferior vena caval obstruction. His edema failed to respond to a combination of diuretics, oral frusemide 40 mg daily and oral spironolactone 100 mg daily. Subcutaneous drainage of both lower limbs with butterfly needles was performed with minimal improvement. However, he gained significant symptomatic relief with multiple subcutaneous punctures and stoma bag drainage. A total of 12.8 L of serous fluid was drained with this simple and effective method. This is the first report of the use of this method.

Matched MeSH terms: Edema/therapy*
Light-Emitting Diode (LED) Therapy Attenuates Neurotoxicity of Methanol-Induced Memory Impairment and Apoptosis in The Hippocampus

Ghanbari A, Zibara K, Salari S, Ghareghani M, Rad P, Mohamed W, et al.

CNS Neurol Disord Drug Targets, 2018;17(7):528-538.
PMID: 29968547 DOI: 10.2174/1871527317666180703111643

BACKGROUND & OBJECTIVE: The adolescent brain has a higher vulnerability to alcoholinduced neurotoxicity, compared to adult's brain. Most studies have investigated the effect of ethanol consumption on the body, however, methanol consumption, which peaked in the last years, is still poorly explored.
METHOD: In this study, we investigated the effects of methanol neurotoxicity on memory function and pathological outcomes in the hippocampus of adolescent rats and examined the efficacy of Light- Emitting Diode (LED) therapy. Methanol induced neurotoxic rats showed a significant decrease in the latency period, in comparison to controls, which was significantly improved in LED treated rats at 7, 14 and 28 days, indicating recovery of memory function. In addition, methanol neurotoxicity in hippocampus caused a significant increase in cell death (caspase3+ cells) and cell edema at 7 and 28 days, which were significantly decreased by LED therapy. Furthermore, the number of glial fibrillary acid protein astrocytes was significantly lower in methanol rats, compared to controls, whereas LED treatment caused their significant increase. Finally, methanol neurotoxicity caused a significant decrease in the number of brain-derived neurotrophic factor (BDNF+) cells, but also circulating serum BDNF, at 7 and 28 days, compared to controls, which were significantly increased by LED therapy. Importantly, LED significantly increased the number of Ki-67+ cells and BDNF levels in the serum and hypothalamus in control-LED rats, compared to controls without LED therapy.
CONCLUSION: In conclusion, chronic methanol administration caused severe memory impairments and several pathological outcomes in the hippocampus of adolescent rats which were improved by LED therapy.

Matched MeSH terms: Brain Edema/therapy